Publications
Publications récentes
2022 |
Worrall WPM Kamphuis JBJ, Stackowicz Mougel Mauré Pecalvel Brûlé Bruhns Guilleminault Reber LL. J A E C S P L The anti-FcεRI antibody MAR-1 depletes basophils and cross-reacts with myeloid cells through its Fc portion Article de journal Allergy, 77 (6), p. 1903-1906, 2022. @article{WPM2022, title = {The anti-FcεRI antibody MAR-1 depletes basophils and cross-reacts with myeloid cells through its Fc portion}, author = {Worrall WPM, Kamphuis JBJ, Stackowicz J, Mougel A, Mauré E, Pecalvel C, Brûlé S, Bruhns P, Guilleminault L, Reber LL.}, url = {https://pubmed.ncbi.nlm.nih.gov/35244223/}, doi = { 10.1111/all.15269}, year = {2022}, date = {2022-06-01}, journal = {Allergy}, volume = {77}, number = {6}, pages = {1903-1906}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Gaudenzio N, Liblau RS. Immune cells impede repair of old neurons Article de journal Science, 376 (6594), p. 694-695, 2022. @article{N2022, title = {Immune cells impede repair of old neurons}, author = {Gaudenzio N, Liblau RS.}, editor = {{Lambert de Rouvroit}, Catherine}, year = {2022}, date = {2022-05-13}, journal = {Science}, volume = {376}, number = {6594}, pages = { 694-695}, abstract = {The regenerative capacity of older people is reduced, resulting in decreased tissue function and resilience. Accordingly, the regeneration of the sciatic nerve after injury has been reported to be less efficient and slower in older people (1). One of the hallmarks of aging is altered intercellular communication, which is often accompanied by increased density of immune cells within tissues and excessive release of proinflammatory mediators, called inflammaging (2, 3). In this context, the immune system disturbs tissue homeostasis and impedes functional recovery. However, the precise mechanisms underlying this pathophysiological process are largely elusive, which is a barrier to rational treatment design. On page 715 of this issue, Zhou et al. (4) describe a mechanism by which aged sensory neurons release the chemoattractive protein C-X-C motif chemokine ligand 13 (CXCL13). Upon sciatic nerve injury in aged, but not young, mice, this results in the recruitment of CD8+ T cells that prevent axonal regeneration.}, keywords = {}, pubstate = {published}, tppubtype = {article} } The regenerative capacity of older people is reduced, resulting in decreased tissue function and resilience. Accordingly, the regeneration of the sciatic nerve after injury has been reported to be less efficient and slower in older people (1). One of the hallmarks of aging is altered intercellular communication, which is often accompanied by increased density of immune cells within tissues and excessive release of proinflammatory mediators, called inflammaging (2, 3). In this context, the immune system disturbs tissue homeostasis and impedes functional recovery. However, the precise mechanisms underlying this pathophysiological process are largely elusive, which is a barrier to rational treatment design. On page 715 of this issue, Zhou et al. (4) describe a mechanism by which aged sensory neurons release the chemoattractive protein C-X-C motif chemokine ligand 13 (CXCL13). Upon sciatic nerve injury in aged, but not young, mice, this results in the recruitment of CD8+ T cells that prevent axonal regeneration. |
Congy-Jolivet, N; Cenac, C; Dellacasagrande, J; Puissant-Lubrano, B; Apoil, P A; Guedj, K; Abbas, F; Laffont, S; Sourdet, S; Guyonnet, S; Nourhashemi, F; Guery, J C; Blancher, A Monocytes are the main source of STING-mediated IFN-alpha production Article de journal EBioMedicine, 80 , p. 104047, 2022, ISSN: 2352-3964 (Electronic) 2352-3964 (Linking). @article{RN2018, title = {Monocytes are the main source of STING-mediated IFN-alpha production}, author = {Congy-Jolivet, N. and Cenac, C. and Dellacasagrande, J. and Puissant-Lubrano, B. and Apoil, P. A. and Guedj, K. and Abbas, F. and Laffont, S. and Sourdet, S. and Guyonnet, S. and Nourhashemi, F. and Guery, J. C. and Blancher, A.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/35561451}, doi = {10.1016/j.ebiom.2022.104047}, issn = {2352-3964 (Electronic) 2352-3964 (Linking)}, year = {2022}, date = {2022-01-01}, journal = {EBioMedicine}, volume = {80}, pages = {104047}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Yang, Cui ; Blaize, Gaëtan ; Marrocco, Rémi ; Rouquié, Nelly ; Bories, Cyrielle ; Gador, Mylène ; Mélique, Suzanne ; Joulia, Emeline ; Benamar, Mehdi ; Dejean, Anne S; Daniels-Treffandier, Hélène ; Love, Paul E; Fazilleau, Nicolas ; Saoudi, Abdelhadi ; Lesourne, Renaud THEMIS enhances the magnitude of normal and neuroinflammatory type 1 immune responses by promoting TCR-independent signals Article de journal Science Signaling, 15 (742), p. eabl5343, 2022, (Publisher: American Association for the Advancement of Science). @article{yang_themis_2022, title = {THEMIS enhances the magnitude of normal and neuroinflammatory type 1 immune responses by promoting TCR-independent signals}, author = {Yang, Cui and Blaize, Gaëtan and Marrocco, Rémi and Rouquié, Nelly and Bories, Cyrielle and Gador, Mylène and Mélique, Suzanne and Joulia, Emeline and Benamar, Mehdi and Dejean, Anne S. and Daniels-Treffandier, Hélène and Love, Paul E. and Fazilleau, Nicolas and Saoudi, Abdelhadi and Lesourne, Renaud}, url = {https://www.science.org/doi/abs/10.1126/scisignal.abl5343}, doi = {10.1126/scisignal.abl5343}, year = {2022}, date = {2022-01-01}, urldate = {2022-07-20}, journal = {Science Signaling}, volume = {15}, number = {742}, pages = {eabl5343}, note = {Publisher: American Association for the Advancement of Science}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Han, Mingyu ; Cantaloube-Ferrieu, Vincent ; Xie, Maorong ; Armani-Tourret, Marie ; Woottum, Marie ; Pagès, Jean-Christophe ; Colin, Philippe ; Lagane, Bernard ; Benichou, Serge HIV-1 cell-to-cell spread overcomes the virus entry block of non-macrophage-tropic strains in macrophages Article de journal PLoS pathogens, 18 (5), p. e1010335, 2022, ISSN: 1553-7374. @article{han_hiv-1_2022, title = {HIV-1 cell-to-cell spread overcomes the virus entry block of non-macrophage-tropic strains in macrophages}, author = {Han, Mingyu and Cantaloube-Ferrieu, Vincent and Xie, Maorong and Armani-Tourret, Marie and Woottum, Marie and Pagès, Jean-Christophe and Colin, Philippe and Lagane, Bernard and Benichou, Serge}, doi = {10.1371/journal.ppat.1010335}, issn = {1553-7374}, year = {2022}, date = {2022-01-01}, journal = {PLoS pathogens}, volume = {18}, number = {5}, pages = {e1010335}, abstract = {Macrophages (MΦ) are increasingly recognized as HIV-1 target cells involved in the pathogenesis and persistence of infection. Paradoxically, in vitro infection assays suggest that virus isolates are mostly T-cell-tropic and rarely MΦ-tropic. The latter are assumed to emerge under CD4+ T-cell paucity in tissues such as the brain or at late stage when the CD4 T-cell count declines. However, assays to qualify HIV-1 tropism use cell-free viral particles and may not fully reflect the conditions of in vivo MΦ infection through cell-to-cell viral transfer. Here, we investigated the capacity of viruses expressing primary envelope glycoproteins (Envs) with CCR5 and/or CXCR4 usage from different stages of infection, including transmitted/founder Envs, to infect MΦ by a cell-free mode and through cell-to-cell transfer from infected CD4+ T cells. The results show that most viruses were unable to enter MΦ as cell-free particles, in agreement with the current view that non-M-tropic viruses inefficiently use CD4 and/or CCR5 or CXCR4 entry receptors on MΦ. In contrast, all viruses could be effectively cell-to-cell transferred to MΦ from infected CD4+ T cells. We further showed that viral transfer proceeded through Env-dependent cell-cell fusion of infected T cells with MΦ targets, leading to the formation of productively infected multinucleated giant cells. Compared to cell-free infection, infected T-cell/MΦ contacts showed enhanced interactions of R5 M- and non-M-tropic Envs with CD4 and CCR5, resulting in a reduced dependence on receptor expression levels on MΦ for viral entry. Altogether, our results show that virus cell-to-cell transfer overcomes the entry block of isolates initially defined as non-macrophage-tropic, indicating that HIV-1 has a more prevalent tropism for MΦ than initially suggested. This sheds light into the role of this route of virus cell-to-cell transfer to MΦ in CD4+ T cell rich tissues for HIV-1 transmission, dissemination and formation of tissue viral reservoirs.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Macrophages (MΦ) are increasingly recognized as HIV-1 target cells involved in the pathogenesis and persistence of infection. Paradoxically, in vitro infection assays suggest that virus isolates are mostly T-cell-tropic and rarely MΦ-tropic. The latter are assumed to emerge under CD4+ T-cell paucity in tissues such as the brain or at late stage when the CD4 T-cell count declines. However, assays to qualify HIV-1 tropism use cell-free viral particles and may not fully reflect the conditions of in vivo MΦ infection through cell-to-cell viral transfer. Here, we investigated the capacity of viruses expressing primary envelope glycoproteins (Envs) with CCR5 and/or CXCR4 usage from different stages of infection, including transmitted/founder Envs, to infect MΦ by a cell-free mode and through cell-to-cell transfer from infected CD4+ T cells. The results show that most viruses were unable to enter MΦ as cell-free particles, in agreement with the current view that non-M-tropic viruses inefficiently use CD4 and/or CCR5 or CXCR4 entry receptors on MΦ. In contrast, all viruses could be effectively cell-to-cell transferred to MΦ from infected CD4+ T cells. We further showed that viral transfer proceeded through Env-dependent cell-cell fusion of infected T cells with MΦ targets, leading to the formation of productively infected multinucleated giant cells. Compared to cell-free infection, infected T-cell/MΦ contacts showed enhanced interactions of R5 M- and non-M-tropic Envs with CD4 and CCR5, resulting in a reduced dependence on receptor expression levels on MΦ for viral entry. Altogether, our results show that virus cell-to-cell transfer overcomes the entry block of isolates initially defined as non-macrophage-tropic, indicating that HIV-1 has a more prevalent tropism for MΦ than initially suggested. This sheds light into the role of this route of virus cell-to-cell transfer to MΦ in CD4+ T cell rich tissues for HIV-1 transmission, dissemination and formation of tissue viral reservoirs. |
Argenty, Jérémy ; Rouquié, Nelly ; Bories, Cyrielle ; Mélique, Suzanne ; Duplan-Eche, Valérie ; Saoudi, Abdelhadi ; Fazilleau, Nicolas ; Lesourne, Renaud A selective LIS1 requirement for mitotic spindle assembly discriminates distinct Ŧ-cell division mechanisms within the Ŧ-cell lineage Article de journal Elife, 11 , p. e80277, 2022, ISSN: 2050-084X. @article{argenty_selective_2022, title = {A selective LIS1 requirement for mitotic spindle assembly discriminates distinct Ŧ-cell division mechanisms within the Ŧ-cell lineage}, author = {Argenty, Jérémy and Rouquié, Nelly and Bories, Cyrielle and Mélique, Suzanne and Duplan-Eche, Valérie and Saoudi, Abdelhadi and Fazilleau, Nicolas and Lesourne, Renaud}, doi = {10.7554/eLife.80277}, issn = {2050-084X}, year = {2022}, date = {2022-01-01}, journal = {Elife}, volume = {11}, pages = {e80277}, abstract = {The ability to proliferate is a common feature of most T-cell populations. However, proliferation follows different cell-cycle dynamics and is coupled to different functional outcomes according to T-cell subsets. Whether the mitotic machineries supporting these qualitatively distinct proliferative responses are identical remains unknown. Here, we show that disruption of the microtubule-associated protein LIS1 in mouse models leads to proliferative defects associated with a blockade of T-cell development after β-selection and of peripheral CD4+ T-cell expansion after antigen priming. In contrast, cell divisions in CD8+ T cells occurred independently of LIS1 following T-cell antigen receptor stimulation, although LIS1 was required for proliferation elicited by pharmacological activation. In thymocytes and CD4+ T cells, LIS1 deficiency did not affect signaling events leading to activation but led to an interruption of proliferation after the initial round of division and to p53-induced cell death. Proliferative defects resulted from a mitotic failure, characterized by the presence of extra-centrosomes and the formation of multipolar spindles, causing abnormal chromosomes congression during metaphase and separation during telophase. LIS1 was required to stabilize dynein/dynactin complexes, which promote chromosome attachment to mitotic spindles and ensure centrosome integrity. Together, these results suggest that proliferative responses are supported by distinct mitotic machineries across T-cell subsets.}, keywords = {}, pubstate = {published}, tppubtype = {article} } The ability to proliferate is a common feature of most T-cell populations. However, proliferation follows different cell-cycle dynamics and is coupled to different functional outcomes according to T-cell subsets. Whether the mitotic machineries supporting these qualitatively distinct proliferative responses are identical remains unknown. Here, we show that disruption of the microtubule-associated protein LIS1 in mouse models leads to proliferative defects associated with a blockade of T-cell development after β-selection and of peripheral CD4+ T-cell expansion after antigen priming. In contrast, cell divisions in CD8+ T cells occurred independently of LIS1 following T-cell antigen receptor stimulation, although LIS1 was required for proliferation elicited by pharmacological activation. In thymocytes and CD4+ T cells, LIS1 deficiency did not affect signaling events leading to activation but led to an interruption of proliferation after the initial round of division and to p53-induced cell death. Proliferative defects resulted from a mitotic failure, characterized by the presence of extra-centrosomes and the formation of multipolar spindles, causing abnormal chromosomes congression during metaphase and separation during telophase. LIS1 was required to stabilize dynein/dynactin complexes, which promote chromosome attachment to mitotic spindles and ensure centrosome integrity. Together, these results suggest that proliferative responses are supported by distinct mitotic machineries across T-cell subsets. |
Giang, N; Villeneuve, T; Maire, K; Mejia, J E; Guery, J C; Pelletier, L; Savignac, M PKCalpha interacts with Ca(v) 1.3 calcium channels to promote the Ca(v) 1.2/Ca(v) 1.3 duo tuning Th2 functions Article de journal Allergy, 2022, ISSN: 1398-9995 (Electronic) 0105-4538 (Linking). @article{RN2049, title = {PKCalpha interacts with Ca(v) 1.3 calcium channels to promote the Ca(v) 1.2/Ca(v) 1.3 duo tuning Th2 functions}, author = {Giang, N. and Villeneuve, T. and Maire, K. and Mejia, J. E. and Guery, J. C. and Pelletier, L. and Savignac, M.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/36478369}, doi = {10.1111/all.15611}, issn = {1398-9995 (Electronic) 0105-4538 (Linking)}, year = {2022}, date = {2022-01-01}, journal = {Allergy}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Giang, N; Mars, M; Moreau, M; Mejia, J E; Bouchaud, G; Magnan, A; Michelet, M; Ronsin, B; Murphy, G G; Striessnig, J; Guery, J C; Pelletier, L; Savignac, M Separation of the Cav1.2-Cav1.3 calcium channel duo prevents type 2 allergic airway inflammation Article de journal Allergy, 77 (2), p. 525-539, 2022, ISSN: 1398-9995 (Electronic) 0105-4538 (Linking). @article{RN1997, title = {Separation of the Cav1.2-Cav1.3 calcium channel duo prevents type 2 allergic airway inflammation}, author = {Giang, N. and Mars, M. and Moreau, M. and Mejia, J. E. and Bouchaud, G. and Magnan, A. and Michelet, M. and Ronsin, B. and Murphy, G. G. and Striessnig, J. and Guery, J. C. and Pelletier, L. and Savignac, M.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/34181765}, doi = {10.1111/all.14993}, issn = {1398-9995 (Electronic) 0105-4538 (Linking)}, year = {2022}, date = {2022-01-01}, journal = {Allergy}, volume = {77}, number = {2}, pages = {525-539}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
2021 |
Marty, FH; Bettamin, L; Thouard, A; Bourgade, K; Allart, S; Larrieu, G; Malnou, CE; Gonzalez-Dunia, D; Suberbielle, E Borna disease virus docks on neuronal DNA double-strand breaks to replicate and dampens neuronal activity Article de journal 2021. @article{2021c, title = {Borna disease virus docks on neuronal DNA double-strand breaks to replicate and dampens neuronal activity}, author = {FH Marty and L Bettamin and A Thouard and K Bourgade and S Allart and G Larrieu and CE Malnou and D Gonzalez-Dunia and E Suberbielle}, editor = {iScience }, doi = {10.1016/j.isci.2021.103621}, year = {2021}, date = {2021-12-16}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Conde E Bertrand R, Balbino Bonnefoy Stackowicz Caillot Colaone Hamdi Houmadi Loste Kamphuis JBJ Huetz Guilleminault Gaudenzio Mougel Hardy Snouwaert JN Koller BH Serra Bruhns Grouard-Vogel Reber LL. B J J N F S R A F L N A D V P G Dual vaccination against IL-4 and IL-13 protects against chronic allergic asthma in mice Article de journal Nature Communications, 12 (1), p. 2574, 2021. @article{E2021, title = {Dual vaccination against IL-4 and IL-13 protects against chronic allergic asthma in mice}, author = {Conde E, Bertrand R, Balbino B, Bonnefoy J, Stackowicz J, Caillot N, Colaone F, Hamdi S, Houmadi R, Loste A, Kamphuis JBJ, Huetz F, Guilleminault L, Gaudenzio N, Mougel A, Hardy D, Snouwaert JN, Koller BH, Serra V, Bruhns P, Grouard-Vogel G, Reber LL.}, doi = {10.1038/s41467-021-22834-5}, year = {2021}, date = {2021-05-11}, journal = {Nature Communications}, volume = {12}, number = {1}, pages = {2574}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Darrigues, Julie ; Santamaria, Jeremy C; Galindo-Albarrán, Ariel ; Robey, Ellen A; Joffre, Olivier P; van Meerwijk, Joost P M; Romagnoli, Paola Robust intrathymic development of regulatory T cells in young NOD mice is rapidly restrained by recirculating cells Article de journal European Journal of Immunology, 2021, ISSN: 15214141. @article{Darrigues2020b, title = {Robust intrathymic development of regulatory T cells in young NOD mice is rapidly restrained by recirculating cells}, author = {Darrigues, Julie and Santamaria, Jeremy C. and Galindo-Albarrán, Ariel and Robey, Ellen A. and Joffre, Olivier P. and van Meerwijk, Joost P.M. and Romagnoli, Paola}, url = {https://pubmed.ncbi.nlm.nih.gov/32730634/}, doi = {10.1002/eji.202048743}, issn = {15214141}, year = {2021}, date = {2021-03-01}, journal = {European Journal of Immunology}, publisher = {Wiley-VCH Verlag}, abstract = {Regulatory T lymphocytes (Treg) play a vital role in the protection of the organism against autoimmune pathology. It is therefore paradoxical that comparatively large numbers of Treg were found in the thymus of type I diabetes-prone NOD mice. The Treg population in the thymus is composed of newly developing cells and cells that had recirculated from the periphery back to the thymus. We here demonstrate that exceptionally large numbers of Treg develop in the thymus of young, but not adult, NOD mice. Once emigrated from the thymus, an unusually large proportion of these Treg is activated in the periphery, which causes a particularly abundant accumulation of recirculating Treg in the thymus. These cells then rapidly inhibit de novo development of Treg. The proportions of developing Treg thus reach levels similar to or lower than those found in most other, type 1 diabetes-resistant, inbred mouse strains. Thus, in adult NOD mice the particularly large Treg-niche is actually composed of mostly recirculating cells and only few newly developing Treg.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Regulatory T lymphocytes (Treg) play a vital role in the protection of the organism against autoimmune pathology. It is therefore paradoxical that comparatively large numbers of Treg were found in the thymus of type I diabetes-prone NOD mice. The Treg population in the thymus is composed of newly developing cells and cells that had recirculated from the periphery back to the thymus. We here demonstrate that exceptionally large numbers of Treg develop in the thymus of young, but not adult, NOD mice. Once emigrated from the thymus, an unusually large proportion of these Treg is activated in the periphery, which causes a particularly abundant accumulation of recirculating Treg in the thymus. These cells then rapidly inhibit de novo development of Treg. The proportions of developing Treg thus reach levels similar to or lower than those found in most other, type 1 diabetes-resistant, inbred mouse strains. Thus, in adult NOD mice the particularly large Treg-niche is actually composed of mostly recirculating cells and only few newly developing Treg. |
El Costa, H; Gouilly, J; Abravanel, F; Bahraoui, E; Peron, J M; Kamar, N; Jabrane-Ferrat, N; Izopet, J Effector memory CD8 T cell response elicits Hepatitis E Virus genotype 3 pathogenesis in the elderly Article de journal PLoS Pathog, 17 (2), p. e1009367, 2021, ISSN: 1553-7374 (Electronic) 1553-7366 (Linking). @article{RN4b, title = {Effector memory CD8 T cell response elicits Hepatitis E Virus genotype 3 pathogenesis in the elderly}, author = {El Costa, H. and Gouilly, J. and Abravanel, F. and Bahraoui, E. and Peron, J. M. and Kamar, N. and Jabrane-Ferrat, N. and Izopet, J.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/33617602}, doi = {10.1371/journal.ppat.1009367}, issn = {1553-7374 (Electronic) 1553-7366 (Linking)}, year = {2021}, date = {2021-01-01}, journal = {PLoS Pathog}, volume = {17}, number = {2}, pages = {e1009367}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Armani-Tourret, M; Zhou, Z; Gasser, R; Staropoli, I; Cantaloube-Ferrieu, V; Benureau, Y; Garcia-Perez, J; Perez-Olmeda, M; Lorin, V; Puissant-Lubrano, B; Assoumou, L; Delaugerre, C; Lelievre, J D; Levy, Y; Mouquet, H; Martin-Blondel, G; Alcami, J; Arenzana-Seisdedos, F; Izopet, J; Colin, P; Lagane, B Mechanisms of HIV-1 evasion to the antiviral activity of chemokine CXCL12 indicate potential links with pathogenesis Article de journal PLoS Pathog, 17 (4), p. e1009526, 2021, ISSN: 1553-7374 (Electronic) 1553-7366 (Linking). @article{RN3b, title = {Mechanisms of HIV-1 evasion to the antiviral activity of chemokine CXCL12 indicate potential links with pathogenesis}, author = {Armani-Tourret, M. and Zhou, Z. and Gasser, R. and Staropoli, I. and Cantaloube-Ferrieu, V. and Benureau, Y. and Garcia-Perez, J. and Perez-Olmeda, M. and Lorin, V. and Puissant-Lubrano, B. and Assoumou, L. and Delaugerre, C. and Lelievre, J. D. and Levy, Y. and Mouquet, H. and Martin-Blondel, G. and Alcami, J. and Arenzana-Seisdedos, F. and Izopet, J. and Colin, P. and Lagane, B.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/33872329}, doi = {10.1371/journal.ppat.1009526}, issn = {1553-7374 (Electronic) 1553-7366 (Linking)}, year = {2021}, date = {2021-01-01}, journal = {PLoS Pathog}, volume = {17}, number = {4}, pages = {e1009526}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Blanquart, E; Mandonnet, A; Mars, M; Cenac, C; Anesi, N; Mercier, P; Audouard, C; Roga, S; Serrano de Almeida, G; Bevan, C L; Girard, J P; Pelletier, L; Laffont, S; Guery, J C Targeting androgen signaling in ILC2s protects from IL-33-driven lung inflammation, independently of KLRG1 Article de journal J Allergy Clin Immunol, 2021, ISSN: 1097-6825 (Electronic) 0091-6749 (Linking). @article{RN1947, title = {Targeting androgen signaling in ILC2s protects from IL-33-driven lung inflammation, independently of KLRG1}, author = {Blanquart, E. and Mandonnet, A. and Mars, M. and Cenac, C. and Anesi, N. and Mercier, P. and Audouard, C. and Roga, S. and Serrano de Almeida, G. and Bevan, C. L. and Girard, J. P. and Pelletier, L. and Laffont, S. and Guery, J. C.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/33964300}, doi = {10.1016/j.jaci.2021.04.029}, issn = {1097-6825 (Electronic) 0091-6749 (Linking)}, year = {2021}, date = {2021-01-01}, journal = {J Allergy Clin Immunol}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Cenac, C; Ducatez, M; Guery, J C Hydroxychloroquine inhibits proteolytic processing of endogenous TLR7 protein in human primary plasmacytoid dendritic cells Article de journal Eur J Immunol, 2021, ISSN: 1521-4141 (Electronic) 0014-2980 (Linking). @article{RN1956, title = {Hydroxychloroquine inhibits proteolytic processing of endogenous TLR7 protein in human primary plasmacytoid dendritic cells}, author = {Cenac, C. and Ducatez, M. and Guery, J. C.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/34580855}, doi = {10.1002/eji.202149361}, issn = {1521-4141 (Electronic) 0014-2980 (Linking)}, year = {2021}, date = {2021-01-01}, journal = {Eur J Immunol}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Osma-Garcia, I C; Capitan-Sobrino, D; Mouysset, M; Bell, S E; Lebeurrier, M; Turner, M; Diaz-Munoz, M D The RNA-binding protein HuR is required for maintenance of the germinal centre response Article de journal Nat Commun, 12 (1), p. 6556, 2021, ISSN: 2041-1723 (Electronic) 2041-1723 (Linking). @article{RN2, title = {The RNA-binding protein HuR is required for maintenance of the germinal centre response}, author = {Osma-Garcia, I. C. and Capitan-Sobrino, D. and Mouysset, M. and Bell, S. E. and Lebeurrier, M. and Turner, M. and Diaz-Munoz, M. D.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/34772950}, doi = {10.1038/s41467-021-26908-2}, issn = {2041-1723 (Electronic) 2041-1723 (Linking)}, year = {2021}, date = {2021-01-01}, journal = {Nat Commun}, volume = {12}, number = {1}, pages = {6556}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Stackowicz, J; Gaudenzio, N; Serhan, N; Conde, E; Godon, O; Marichal, T; Starkl, P; Balbino, B; Roers, A; Bruhns, P; Jonsson, F; Moguelet, P; Georgin-Lavialle, S; Broderick, L; Hoffman, H M; Galli, S J; Reber, L L Neutrophil-specific gain-of-function mutations in Nlrp3 promote development of cryopyrin-associated periodic syndrome Article de journal J Exp Med, 218 (10), 2021, ISSN: 1540-9538 (Electronic) 0022-1007 (Linking). @article{RN2330, title = {Neutrophil-specific gain-of-function mutations in Nlrp3 promote development of cryopyrin-associated periodic syndrome}, author = {Stackowicz, J. and Gaudenzio, N. and Serhan, N. and Conde, E. and Godon, O. and Marichal, T. and Starkl, P. and Balbino, B. and Roers, A. and Bruhns, P. and Jonsson, F. and Moguelet, P. and Georgin-Lavialle, S. and Broderick, L. and Hoffman, H. M. and Galli, S. J. and Reber, L. L.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/34477811}, doi = {10.1084/jem.20201466}, issn = {1540-9538 (Electronic) 0022-1007 (Linking)}, year = {2021}, date = {2021-01-01}, journal = {J Exp Med}, volume = {218}, number = {10}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
2020 |
Briand-M{é}sange, Fabienne ; Pons, V{é}ronique ; Allart, Sophie ; Masquelier, Julien ; Chicanne, Ga{ë}tan ; Beton, Nicolas ; Payrastre, Bernard ; Muccioli, Giulio G; Ausseil, J{é}r{ô}me ; Davignon, Jean Luc ; Salles, Jean Pierre ; Chap, Hugues Glycerophosphodiesterase 3 (GDE3) is a lysophosphatidylinositol-specific ectophospholipase C acting as an endocannabinoid signaling switch Article de journal Journal of Biological Chemistry, 295 (46), p. 15767–15781, 2020, ISSN: 1083351X. @article{Briand-Mesange2020, title = {Glycerophosphodiesterase 3 (GDE3) is a lysophosphatidylinositol-specific ectophospholipase C acting as an endocannabinoid signaling switch}, author = {Briand-M{é}sange, Fabienne and Pons, V{é}ronique and Allart, Sophie and Masquelier, Julien and Chicanne, Ga{ë}tan and Beton, Nicolas and Payrastre, Bernard and Muccioli, Giulio G. and Ausseil, J{é}r{ô}me and Davignon, Jean Luc and Salles, Jean Pierre and Chap, Hugues}, doi = {10.1074/jbc.RA120.015278}, issn = {1083351X}, year = {2020}, date = {2020-11-01}, journal = {Journal of Biological Chemistry}, volume = {295}, number = {46}, pages = {15767--15781}, publisher = {American Society for Biochemistry and Molecular Biology Inc.}, abstract = {Endocannabinoid signaling plays a regulatory role in various (neuro)biological functions. 2-arachidonoylglycerol (2-AG) is the most abundant endocannabinoid, and although its canonical biosynthetic pathway involving phosphoinositide-specific phospholipase C and diacylglycerol lipase a is known, alternative pathways remain unsettled. Here, we characterize a non-canonical pathway implicating glycerophosphodiesterase 3 (GDE3, from GDPD2 gene). Human GDE3 expressed in HEK293T cell membranes catalyzed the conversion of lysophosphatidylinositol (LPI) into monoacylglycerol and inositol-1-phosphate. The enzyme was equally active against 1-acyl and 2-acyl LPI. When using 2-acyl LPI, where arachidonic acid is the predominant fatty acid, LC-MS analysis identified 2-AG as the main product of LPI hydrolysis by GDE3. Furthermore, inositol-1-phosphate release into the medium occurred upon addition of LPI to intact cells, suggesting that GDE3 is actually an ecto-lysophospholipase C. In cells expressing G-protein–coupled receptor GPR55, GDE3 abolished 1-acyl LPI–induced signaling. In contrast, upon simultaneous expression of GDE3 and cannabinoid receptor CB2, 2-acyl LPI evoked the same signal as that induced by 2-AG. These data strongly suggest that, in addition to degrading the GPR55 LPI ligand, GDE3 can act as a switch between GPR55 and CB2 signaling. Coincident with a major expression of both GDE3 and CB2 in the spleen, spleens from transgenic mice lacking GDE3 displayed doubling of LPI content compared with WT mice. Decreased production of 2-AG in whole spleen was also observed, supporting the in vivo relevance of our findings. These data thus open a new research avenue in the field of endocannabinoid generation and reinforce the view of GPR55 and LPI being genuine actors of the endocannabinoid system.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Endocannabinoid signaling plays a regulatory role in various (neuro)biological functions. 2-arachidonoylglycerol (2-AG) is the most abundant endocannabinoid, and although its canonical biosynthetic pathway involving phosphoinositide-specific phospholipase C and diacylglycerol lipase a is known, alternative pathways remain unsettled. Here, we characterize a non-canonical pathway implicating glycerophosphodiesterase 3 (GDE3, from GDPD2 gene). Human GDE3 expressed in HEK293T cell membranes catalyzed the conversion of lysophosphatidylinositol (LPI) into monoacylglycerol and inositol-1-phosphate. The enzyme was equally active against 1-acyl and 2-acyl LPI. When using 2-acyl LPI, where arachidonic acid is the predominant fatty acid, LC-MS analysis identified 2-AG as the main product of LPI hydrolysis by GDE3. Furthermore, inositol-1-phosphate release into the medium occurred upon addition of LPI to intact cells, suggesting that GDE3 is actually an ecto-lysophospholipase C. In cells expressing G-protein–coupled receptor GPR55, GDE3 abolished 1-acyl LPI–induced signaling. In contrast, upon simultaneous expression of GDE3 and cannabinoid receptor CB2, 2-acyl LPI evoked the same signal as that induced by 2-AG. These data strongly suggest that, in addition to degrading the GPR55 LPI ligand, GDE3 can act as a switch between GPR55 and CB2 signaling. Coincident with a major expression of both GDE3 and CB2 in the spleen, spleens from transgenic mice lacking GDE3 displayed doubling of LPI content compared with WT mice. Decreased production of 2-AG in whole spleen was also observed, supporting the in vivo relevance of our findings. These data thus open a new research avenue in the field of endocannabinoid generation and reinforce the view of GPR55 and LPI being genuine actors of the endocannabinoid system. |
Balbino, B; Herviou, P; o Godon,; Stackowicz, J; Goff, O R; Iannascoli, B; Sterlin, D; Brûlé, S; Millot, G A; Harris, F M; Voronina, V A; Nadeau, K C; Macdonald, L E; Murphy, A J; Bruhns, P; Reber, L L The anti-IgE mAb omalizumab induces adverse reactions by engaging Fcγ receptors. Article de journal J Clin Invest, 130 (3), p. 1330-1335, 2020. @article{B2020, title = {The anti-IgE mAb omalizumab induces adverse reactions by engaging Fcγ receptors.}, author = {B Balbino and P Herviou and o Godon and J Stackowicz and O R Goff and B Iannascoli and D Sterlin and S Brûlé and G A Millot and F M Harris and V A Voronina and K C Nadeau and L E Macdonald and A J Murphy and P Bruhns and L L Reber}, url = {https://pubmed-ncbi-nlm-nih-gov.proxy.insermbiblio.inist.fr/31770111/}, doi = {10.1172/JCI129697}, year = {2020}, date = {2020-03-02}, journal = {J Clin Invest}, volume = {130}, number = {3}, pages = {1330-1335}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Meixiong, James ; Basso, Lilian ; Dong, Xinzhong ; Gaudenzio, Nicolas Nociceptor-Mast Cell Sensory Clusters as Regulators of Skin Homeostasis. Article de journal Trends in neurosciences, 43 (3), p. 130–132, 2020, ISSN: 1878-108X (Electronic). @article{Meixiong2020, title = {Nociceptor-Mast Cell Sensory Clusters as Regulators of Skin Homeostasis.}, author = {Meixiong, James and Basso, Lilian and Dong, Xinzhong and Gaudenzio, Nicolas}, doi = {10.1016/j.tins.2020.01.001}, issn = {1878-108X (Electronic)}, year = {2020}, date = {2020-03-01}, journal = {Trends in neurosciences}, volume = {43}, number = {3}, pages = {130--132}, abstract = {Recent studies revealed the existence of unique functional links between mast cells and nociceptors in the skin. Here, we propose that mast cells and nociceptors form a single regulatory unit in both physiology and disease. In this model, MrgprB2/X2 signaling is a primary mechanism by which mast cells functionally interact with nociceptors to form specialized neuroimmune clusters that regulate pain, inflammation, and itch.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Recent studies revealed the existence of unique functional links between mast cells and nociceptors in the skin. Here, we propose that mast cells and nociceptors form a single regulatory unit in both physiology and disease. In this model, MrgprB2/X2 signaling is a primary mechanism by which mast cells functionally interact with nociceptors to form specialized neuroimmune clusters that regulate pain, inflammation, and itch. |
Hassan, A; Wlodarczyk, M F; Benamar, M; Bassot, E; Salvioni, A; Kassem, S; Berry, A; Saoudi, A; Blanchard, N A Virus Hosted in Malaria-Infected Blood Protects against T Cell-Mediated Inflammatory Diseases by Impairing DC Function in a Type I IFN-Dependent Manner Article de journal mBio, 11 (2), 2020, (doi: 10.1128/mBio.03394-19.). @article{c, title = {A Virus Hosted in Malaria-Infected Blood Protects against T Cell-Mediated Inflammatory Diseases by Impairing DC Function in a Type I IFN-Dependent Manner}, author = {Hassan, A. and Wlodarczyk, M. F. and Benamar, M. and Bassot, E. and Salvioni, A. and Kassem, S. and Berry, A. and Saoudi, A. and Blanchard, N.}, year = {2020}, date = {2020-01-01}, journal = {mBio}, volume = {11}, number = {2}, abstract = {Coinfections shape immunity and influence the development of inflammatory diseases, resulting in detrimental or beneficial outcome. Coinfections with concurrent Plasmodium species can alter malaria clinical evolution, and malaria infection itself can modulate autoimmune reactions. Yet, the underlying mechanisms remain ill defined. Here, we demonstrate that the protective effects of some rodent malaria strains on T cell-mediated inflammatory pathologies are due to an RNA virus cohosted in malaria-parasitized blood. We show that live and extracts of blood parasitized by Plasmodium berghei K173 or Plasmodium yoelii 17X YM, protect against P. berghei ANKA-induced experimental cerebral malaria (ECM) and myelin oligodendrocyte glycoprotein (MOG)/complete Freund's adjuvant (CFA)-induced experimental autoimmune encephalomyelitis (EAE), and that protection is associated with a strong type I interferon (IFN-I) signature. We detected the presence of the RNA virus lactate dehydrogenase-elevating virus (LDV) in the protective Plasmodium stabilates and we established that LDV infection alone was necessary and sufficient to recapitulate the protective effects on ECM and EAE. In ECM, protection resulted from an IFN-I-mediated reduction in the abundance of splenic conventional dendritic cell and impairment of their ability to produce interleukin (IL)-12p70, leading to a decrease in pathogenic CD4(+) Th1 responses. In EAE, LDV infection induced IFN-I-mediated abrogation of IL-23, thereby preventing the differentiation of granulocyte-macrophage colony-stimulating factor (GM-CSF)-producing encephalitogenic CD4(+) T cells. Our work identifies a virus cohosted in several Plasmodium stabilates across the community and deciphers its major consequences on the host immune system. More generally, our data emphasize the importance of considering contemporaneous infections for the understanding of malaria-associated and autoimmune diseases.IMPORTANCE Any infection modifies the host immune status, potentially ameliorating or aggravating the pathophysiology of a simultaneous inflammatory condition. In the course of investigating how malaria infection modulates the severity of contemporaneous inflammatory diseases, we identified a nonpathogenic mouse virus in stabilates of two widely used rodent parasite lines: Plasmodium berghei K173 and Plasmodium yoelii 17X YM. We established that the protective effects of these Plasmodium lines on cerebral malaria and multiple sclerosis are exclusively due to this virus. The virus induces a massive type I interferon (IFN-I) response and causes quantitative and qualitative defects in the ability of dendritic cells to promote pathogenic T cell responses. Beyond revealing a possible confounding factor in rodent malaria models, our work uncovers some bases by which a seemingly innocuous viral (co)infection profoundly changes the immunopathophysiology of inflammatory diseases.}, note = {doi: 10.1128/mBio.03394-19.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Coinfections shape immunity and influence the development of inflammatory diseases, resulting in detrimental or beneficial outcome. Coinfections with concurrent Plasmodium species can alter malaria clinical evolution, and malaria infection itself can modulate autoimmune reactions. Yet, the underlying mechanisms remain ill defined. Here, we demonstrate that the protective effects of some rodent malaria strains on T cell-mediated inflammatory pathologies are due to an RNA virus cohosted in malaria-parasitized blood. We show that live and extracts of blood parasitized by Plasmodium berghei K173 or Plasmodium yoelii 17X YM, protect against P. berghei ANKA-induced experimental cerebral malaria (ECM) and myelin oligodendrocyte glycoprotein (MOG)/complete Freund's adjuvant (CFA)-induced experimental autoimmune encephalomyelitis (EAE), and that protection is associated with a strong type I interferon (IFN-I) signature. We detected the presence of the RNA virus lactate dehydrogenase-elevating virus (LDV) in the protective Plasmodium stabilates and we established that LDV infection alone was necessary and sufficient to recapitulate the protective effects on ECM and EAE. In ECM, protection resulted from an IFN-I-mediated reduction in the abundance of splenic conventional dendritic cell and impairment of their ability to produce interleukin (IL)-12p70, leading to a decrease in pathogenic CD4(+) Th1 responses. In EAE, LDV infection induced IFN-I-mediated abrogation of IL-23, thereby preventing the differentiation of granulocyte-macrophage colony-stimulating factor (GM-CSF)-producing encephalitogenic CD4(+) T cells. Our work identifies a virus cohosted in several Plasmodium stabilates across the community and deciphers its major consequences on the host immune system. More generally, our data emphasize the importance of considering contemporaneous infections for the understanding of malaria-associated and autoimmune diseases.IMPORTANCE Any infection modifies the host immune status, potentially ameliorating or aggravating the pathophysiology of a simultaneous inflammatory condition. In the course of investigating how malaria infection modulates the severity of contemporaneous inflammatory diseases, we identified a nonpathogenic mouse virus in stabilates of two widely used rodent parasite lines: Plasmodium berghei K173 and Plasmodium yoelii 17X YM. We established that the protective effects of these Plasmodium lines on cerebral malaria and multiple sclerosis are exclusively due to this virus. The virus induces a massive type I interferon (IFN-I) response and causes quantitative and qualitative defects in the ability of dendritic cells to promote pathogenic T cell responses. Beyond revealing a possible confounding factor in rodent malaria models, our work uncovers some bases by which a seemingly innocuous viral (co)infection profoundly changes the immunopathophysiology of inflammatory diseases. |
Lamsoul, Isabelle ; Dupré, Loïc ; Lutz, Pierre G Molecular Tuning of Filamin A Activities in the Context of Adhesion and Migration Article de journal Front Cell Dev Biol, 8 , p. 591323, 2020, ISSN: 2296-634X. @article{lamsoul_molecular_2020, title = {Molecular Tuning of Filamin A Activities in the Context of Adhesion and Migration}, author = {Lamsoul, Isabelle and Dupré, Loïc and Lutz, Pierre G.}, doi = {10.3389/fcell.2020.591323}, issn = {2296-634X}, year = {2020}, date = {2020-01-01}, journal = {Front Cell Dev Biol}, volume = {8}, pages = {591323}, abstract = {The dynamic organization of actin cytoskeleton meshworks relies on multiple actin-binding proteins endowed with distinct actin-remodeling activities. Filamin A is a large multi-domain scaffolding protein that cross-links actin filaments with orthogonal orientation in response to various stimuli. As such it plays key roles in the modulation of cell shape, cell motility, and differentiation throughout development and adult life. The essentiality and complexity of Filamin A is highlighted by mutations that lead to a variety of severe human disorders affecting multiple organs. One of the most conserved activity of Filamin A is to bridge the actin cytoskeleton to integrins, thereby maintaining the later in an inactive state. We here review the numerous mechanisms cells have developed to adjust Filamin A content and activity and focus on the function of Filamin A as a gatekeeper to integrin activation and associated adhesion and motility.}, keywords = {}, pubstate = {published}, tppubtype = {article} } The dynamic organization of actin cytoskeleton meshworks relies on multiple actin-binding proteins endowed with distinct actin-remodeling activities. Filamin A is a large multi-domain scaffolding protein that cross-links actin filaments with orthogonal orientation in response to various stimuli. As such it plays key roles in the modulation of cell shape, cell motility, and differentiation throughout development and adult life. The essentiality and complexity of Filamin A is highlighted by mutations that lead to a variety of severe human disorders affecting multiple organs. One of the most conserved activity of Filamin A is to bridge the actin cytoskeleton to integrins, thereby maintaining the later in an inactive state. We here review the numerous mechanisms cells have developed to adjust Filamin A content and activity and focus on the function of Filamin A as a gatekeeper to integrin activation and associated adhesion and motility. |
Azar, P; Mejía, J E; Cenac, C; Shaiykova, A; Youness, A; Laffont, S; Essat, A; Izopet, J; Passaes, C; Müller-Trutwin, M; Delobel, P; Meyer, L; Guéry, J C TLR7 dosage polymorphism shapes interferogenesis and HIV-1 acute viremia in women Article de journal JCI Insight, 5 (12), 2020, ISSN: 2379-3708. @article{RN1940, title = {TLR7 dosage polymorphism shapes interferogenesis and HIV-1 acute viremia in women}, author = {Azar, P. and Mejía, J. E. and Cenac, C. and Shaiykova, A. and Youness, A. and Laffont, S. and Essat, A. and Izopet, J. and Passaes, C. and Müller-Trutwin, M. and Delobel, P. and Meyer, L. and Guéry, J. C.}, doi = {10.1172/jci.insight.136047}, issn = {2379-3708}, year = {2020}, date = {2020-01-01}, journal = {JCI Insight}, volume = {5}, number = {12}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Raymond, Stéphanie ; Piffaut, Marie ; Bigot, Jonathan ; Cazabat, Michelle ; Montes, Brigitte ; Bertrand, Kevin ; Martin-Blondel, Guillaume ; Izopet, Jacques ; Delobel, Pierre Sexual transmission of an extensively drug-resistant HIV-1 strain Article de journal The Lancet HIV, 7 (8), p. e529–e530, 2020, ISSN: 23523018. @article{raymond_sexual_2020, title = {Sexual transmission of an extensively drug-resistant HIV-1 strain}, author = {Raymond, Stéphanie and Piffaut, Marie and Bigot, Jonathan and Cazabat, Michelle and Montes, Brigitte and Bertrand, Kevin and Martin-Blondel, Guillaume and Izopet, Jacques and Delobel, Pierre}, url = {https://linkinghub.elsevier.com/retrieve/pii/S2352301820302058}, doi = {10.1016/S2352-3018(20)30205-8}, issn = {23523018}, year = {2020}, date = {2020-01-01}, urldate = {2021-02-09}, journal = {The Lancet HIV}, volume = {7}, number = {8}, pages = {e529--e530}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Nayrac, Manon ; Requena, Mary ; Loiseau, Claire ; Cazabat, Michelle ; Suc, Bertrand ; Carrere, Nicolas ; Barange, Karl ; Alric, Laurent ; Martin-Blondel, Guillaume ; Izopet, Jacques ; Delobel, Pierre Th22 cells are efficiently recruited in the gut by CCL28 as an alternative to CCL20 but do not compensate for the loss of Th17 cells in treated HIV-1-infected individuals Article de journal Mucosal Immunology, 14 (1), p. 219–228, 2020, ISSN: 1933-0219, 1935-3456. @article{nayrac_th22_2020, title = {Th22 cells are efficiently recruited in the gut by CCL28 as an alternative to CCL20 but do not compensate for the loss of Th17 cells in treated HIV-1-infected individuals}, author = {Nayrac, Manon and Requena, Mary and Loiseau, Claire and Cazabat, Michelle and Suc, Bertrand and Carrere, Nicolas and Barange, Karl and Alric, Laurent and Martin-Blondel, Guillaume and Izopet, Jacques and Delobel, Pierre}, url = {http://www.nature.com/articles/s41385-020-0286-6}, doi = {10.1038/s41385-020-0286-6}, issn = {1933-0219, 1935-3456}, year = {2020}, date = {2020-01-01}, urldate = {2021-02-09}, journal = {Mucosal Immunology}, volume = {14}, number = {1}, pages = {219--228}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Marion, Olivier ; Lhomme, Sebastien ; Nayrac, Manon ; Dubois, Martine ; Pucelle, Mélanie ; Requena, Mary ; Migueres, Marion ; Abravanel, Florence ; Peron, Jean Marie ; Carrere, Nicolas ; Suc, Bertrand ; Delobel, Pierre ; Kamar, Nassim ; Izopet, Jacques Hepatitis E virus replication in human intestinal cells Article de journal Gut, 69 (5), p. 901–910, 2020, ISSN: 0017-5749, 1468-3288. @article{marion_hepatitis_2020, title = {Hepatitis E virus replication in human intestinal cells}, author = {Marion, Olivier and Lhomme, Sebastien and Nayrac, Manon and Dubois, Martine and Pucelle, Mélanie and Requena, Mary and Migueres, Marion and Abravanel, Florence and Peron, Jean Marie and Carrere, Nicolas and Suc, Bertrand and Delobel, Pierre and Kamar, Nassim and Izopet, Jacques}, url = {https://gut.bmj.com/lookup/doi/10.1136/gutjnl-2019-319004}, doi = {10.1136/gutjnl-2019-319004}, issn = {0017-5749, 1468-3288}, year = {2020}, date = {2020-01-01}, urldate = {2021-02-09}, journal = {Gut}, volume = {69}, number = {5}, pages = {901--910}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Chen, Qian ; Gouilly, Jordi ; Ferrat, Yann J; Espino, Ana ; Glaziou, Quentin ; Cartron, Géraldine ; El Costa, Hicham ; Al-Daccak, Reem ; Jabrane-Ferrat, Nabila Metabolic reprogramming by Zika virus provokes inflammation in human placenta Article de journal Nature Communications, 11 (1), 2020, ISSN: 2041-1723. @article{chen_metabolic_2020, title = {Metabolic reprogramming by Zika virus provokes inflammation in human placenta}, author = {Chen, Qian and Gouilly, Jordi and Ferrat, Yann J. and Espino, Ana and Glaziou, Quentin and Cartron, Géraldine and El Costa, Hicham and Al-Daccak, Reem and Jabrane-Ferrat, Nabila}, url = {http://www.nature.com/articles/s41467-020-16754-z}, doi = {10.1038/s41467-020-16754-z}, issn = {2041-1723}, year = {2020}, date = {2020-01-01}, urldate = {2021-02-09}, journal = {Nature Communications}, volume = {11}, number = {1}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Malviya, M; Saoudi, A; Bauer, J; Fillatreau, S; Liblau, R Treatment of experimental autoimmune encephalomyelitis with engineered bi-specific Foxp3+ regulatory CD4+ T cells Article de journal J Autoimmun, 108 , p. 102401, 2020, ISSN: 1095-9157 (Electronic) 0896-8411 (Linking). @article{RN54, title = {Treatment of experimental autoimmune encephalomyelitis with engineered bi-specific Foxp3+ regulatory CD4+ T cells}, author = {Malviya, M. and Saoudi, A. and Bauer, J. and Fillatreau, S. and Liblau, R.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/31948790}, doi = {10.1016/j.jaut.2020.102401}, issn = {1095-9157 (Electronic) 0896-8411 (Linking)}, year = {2020}, date = {2020-01-01}, journal = {J Autoimmun}, volume = {108}, pages = {102401}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
2019 |
Serhan, N; Basso, L; Sibilano, R; Petitfils, C; Meixiong, J; Bonnart, C; Reber, L L; Marichal, T; Starkl, P; Cenac, N; Dong, X; Tsai, M; Galli, S J; Gaudenzio, N House dust mites activate nociceptor-mast cell clusters to drive type 2 skin inflammation Article de journal Nat Immunol, 20 (11), p. 1435-1443, 2019. @article{N2019, title = {House dust mites activate nociceptor-mast cell clusters to drive type 2 skin inflammation}, author = {Serhan, N. and Basso, L. and Sibilano, R. and Petitfils, C. and Meixiong, J. and Bonnart, C. and Reber, L L. and Marichal, T. and Starkl, P. and Cenac, N. and Dong, X. and Tsai, M. and Galli, S J. and Gaudenzio, N.}, url = {https://pubmed-ncbi-nlm-nih-gov.proxy.insermbiblio.inist.fr/31591569/}, doi = {10.1038/s41590-019-0493-z}, year = {2019}, date = {2019-11-20}, journal = {Nat Immunol}, volume = {20}, number = {11}, pages = {1435-1443}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Adoue, V; Binet, B; Malbec, A; Fourquet, J; Romagnoli, P; van Meerwijk, J P M; Amigorena, S; Joffre, O P The Histone Methyltransferase SETDB1 Controls T Helper Cell Lineage Integrity by Repressing Endogenous Retroviruses. Article de journal Immunity, 50 , p. 629–644, 2019. @article{Adoue2019, title = {The Histone Methyltransferase SETDB1 Controls T Helper Cell Lineage Integrity by Repressing Endogenous Retroviruses.}, author = {Adoue, V and Binet, B and Malbec, A and Fourquet, J and Romagnoli, P and van Meerwijk, J P M and Amigorena, S and Joffre, O P}, url = {https://linkinghub.elsevier.com/retrieve/pii/S1074761319300032}, doi = {10.1016/j.immuni.2019.01.003}, year = {2019}, date = {2019-01-01}, journal = {Immunity}, volume = {50}, pages = {629--644}, abstract = {Upon activation, naive CD4+ T cells differentiate into distinct T cell subsets via processes reliant on epigenetically regulated, lineage-specific developmental programs. Here, we examined the function of the histone methyltransferase SETDB1 in T helper (Th) cell differentiation. Setdb1-/- naive CD4+ T cells exhibited exacerbated Th1 priming, and when exposed to a Th1-instructive signal, Setdb1-/- Th2 cells crossed lineage boundaries and acquired a Th1 phenotype. SETDB1 did not directly control Th1 gene promoter activity but relied instead on deposition of the repressive H3K9me3 mark at a restricted and cell-type-specific set of endogenous retroviruses (ERVs) located in the vicinity of genes involved in immune processes. Refined bioinformatic analyses suggest that these retrotransposons regulate Th1 gene cis-regulatory elements or act as Th1 gene enhancers. Thus, H3K9me3 deposition by SETDB1 ensures Th cell lineage integrity by repressing a repertoire of ERVs that have been exapted into cis-regulatory modules to shape and control the Th1 gene network.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Upon activation, naive CD4+ T cells differentiate into distinct T cell subsets via processes reliant on epigenetically regulated, lineage-specific developmental programs. Here, we examined the function of the histone methyltransferase SETDB1 in T helper (Th) cell differentiation. Setdb1-/- naive CD4+ T cells exhibited exacerbated Th1 priming, and when exposed to a Th1-instructive signal, Setdb1-/- Th2 cells crossed lineage boundaries and acquired a Th1 phenotype. SETDB1 did not directly control Th1 gene promoter activity but relied instead on deposition of the repressive H3K9me3 mark at a restricted and cell-type-specific set of endogenous retroviruses (ERVs) located in the vicinity of genes involved in immune processes. Refined bioinformatic analyses suggest that these retrotransposons regulate Th1 gene cis-regulatory elements or act as Th1 gene enhancers. Thus, H3K9me3 deposition by SETDB1 ensures Th cell lineage integrity by repressing a repertoire of ERVs that have been exapted into cis-regulatory modules to shape and control the Th1 gene network. |
Domingo, Cristina ; Fraissinet, Juliane ; Ansah, Patrick O; Kelly, Corey ; Bhat, Niranjan ; Sow, Samba O; Mejía, José E Long-term immunity against yellow fever in children vaccinated during infancy: a longitudinal cohort study Article de journal Lancet Infect Dis, 2019, ISSN: 1473-3099. @article{RN3090, title = {Long-term immunity against yellow fever in children vaccinated during infancy: a longitudinal cohort study}, author = {Domingo, Cristina and Fraissinet, Juliane and Ansah, Patrick O. and Kelly, Corey and Bhat, Niranjan and Sow, Samba O. and Mejía, José E.}, doi = {10.1016/S1473-3099(19)30323-8}, issn = {1473-3099}, year = {2019}, date = {2019-01-01}, journal = {Lancet Infect Dis}, abstract = {Background. A single dose of vaccine against yellow fever is routinely administered to infants aged 9–12 months under the Expanded Programme on Immunization, but the long-term outcome of vaccination in this age group is unknown. We aimed to evaluate the long-term persistence of neutralising antibodies to yellow fever virus following routine vaccination in infancy. Methods. We did a longitudinal cohort study, using a microneutralisation assay to measure protective antibodies against yellow fever in Malian and Ghanaian children vaccinated around age 9 months and followed up for 4·5 years (Mali), or 2·3 and 6·0 years (Ghana). Healthy children with available day-0 sera, a complete follow-up history, and no record of yellow fever revaccination were included; children seropositive for yellow fever at baseline were excluded. We standardised antibody concentrations with reference to the yellow fever WHO International Standard. Findings. We included 587 Malian and 436 Ghanaian children vaccinated between June 5, 2009, and Dec 26, 2012. In the Malian group, 296 (50·4%, 95% CI 46·4–54·5) were seropositive (antibody concentration ≥0·5 IU/mL) 4·5 years after vaccination. Among the Ghanaian children, 121 (27·8%, 23·5–32·0) were seropositive after 2·3 years. These results show a large decrease from the proportions of seropositive infants 28 days after vaccination, 96·7% in Mali and 72·7% in Ghana, reported by a previous study of both study populations. The number of seropositive children increased to 188 (43·1%, 95% CI 38·5–47·8) in the Ghanaian group 6·0 years after vaccination, but this result might be confounded by unrecorded revaccination or natural infection with wild yellow fever virus during a 2011–12 outbreak in northern Ghana. Interpretation. Rapid waning of immunity during the early years after vaccination of 9-month-old infants argues for a revision of the single-dose recommendation for this target population in endemic countries. The short duration of immunity in many vaccinees suggests that booster vaccination is necessary to meet the 80% population immunity threshold for prevention of yellow fever outbreaks. }, keywords = {}, pubstate = {published}, tppubtype = {article} } Background. A single dose of vaccine against yellow fever is routinely administered to infants aged 9–12 months under the Expanded Programme on Immunization, but the long-term outcome of vaccination in this age group is unknown. We aimed to evaluate the long-term persistence of neutralising antibodies to yellow fever virus following routine vaccination in infancy. Methods. We did a longitudinal cohort study, using a microneutralisation assay to measure protective antibodies against yellow fever in Malian and Ghanaian children vaccinated around age 9 months and followed up for 4·5 years (Mali), or 2·3 and 6·0 years (Ghana). Healthy children with available day-0 sera, a complete follow-up history, and no record of yellow fever revaccination were included; children seropositive for yellow fever at baseline were excluded. We standardised antibody concentrations with reference to the yellow fever WHO International Standard. Findings. We included 587 Malian and 436 Ghanaian children vaccinated between June 5, 2009, and Dec 26, 2012. In the Malian group, 296 (50·4%, 95% CI 46·4–54·5) were seropositive (antibody concentration ≥0·5 IU/mL) 4·5 years after vaccination. Among the Ghanaian children, 121 (27·8%, 23·5–32·0) were seropositive after 2·3 years. These results show a large decrease from the proportions of seropositive infants 28 days after vaccination, 96·7% in Mali and 72·7% in Ghana, reported by a previous study of both study populations. The number of seropositive children increased to 188 (43·1%, 95% CI 38·5–47·8) in the Ghanaian group 6·0 years after vaccination, but this result might be confounded by unrecorded revaccination or natural infection with wild yellow fever virus during a 2011–12 outbreak in northern Ghana. Interpretation. Rapid waning of immunity during the early years after vaccination of 9-month-old infants argues for a revision of the single-dose recommendation for this target population in endemic countries. The short duration of immunity in many vaccinees suggests that booster vaccination is necessary to meet the 80% population immunity threshold for prevention of yellow fever outbreaks. |
Piliponsky, A M; Shubin, N J; Lahiri, A K; Truong, P; Clauson, M; Niino, K; Tsuha, A L; Nedospasov, S A; Karasuyama, H; Reber, L L; Tsai, M; Mukai, K; Galli, S J Basophil-derived tumor necrosis factor can enhance survival in a sepsis model in mice Article de journal Nat Immunol, 20 (2), p. 129-140, 2019, ISSN: 1529-2916 (Electronic) 1529-2908 (Linking). @article{RN1b, title = {Basophil-derived tumor necrosis factor can enhance survival in a sepsis model in mice}, author = {Piliponsky, A. M. and Shubin, N. J. and Lahiri, A. K. and Truong, P. and Clauson, M. and Niino, K. and Tsuha, A. L. and Nedospasov, S. A. and Karasuyama, H. and Reber, L. L. and Tsai, M. and Mukai, K. and Galli, S. J.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/30664762}, doi = {10.1038/s41590-018-0288-7}, issn = {1529-2916 (Electronic) 1529-2908 (Linking)}, year = {2019}, date = {2019-01-01}, journal = {Nat Immunol}, volume = {20}, number = {2}, pages = {129-140}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
2018 |
Rosa, N; Triffaux, E; Robert, V; Mars, M; Klein, M; Bouchaud, G; Canivet, A; Magnan, A; Guery, J C; Pelletier, L; Savignac, M The beta and alpha2delta auxiliary subunits of voltage-gated calcium channel 1 (Cav1) are required for TH2 lymphocyte function and acute allergic airway inflammation Article de journal J Allergy Clin Immunol, 142 (3), p. 892-903, 2018, ISSN: 1097-6825 (Electronic) 0091-6749 (Linking). @article{RN24, title = {The beta and alpha2delta auxiliary subunits of voltage-gated calcium channel 1 (Cav1) are required for TH2 lymphocyte function and acute allergic airway inflammation}, author = {Rosa, N. and Triffaux, E. and Robert, V. and Mars, M. and Klein, M. and Bouchaud, G. and Canivet, A. and Magnan, A. and Guery, J. C. and Pelletier, L. and Savignac, M.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/29129580 https://www.sciencedirect.com/science/article/pii/S0091674917317402}, doi = {10.1016/j.jaci.2017.09.045}, issn = {1097-6825 (Electronic) 0091-6749 (Linking)}, year = {2018}, date = {2018-09-01}, journal = {J Allergy Clin Immunol}, volume = {142}, number = {3}, pages = {892-903}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Souyris, M; Cenac, C; Azar, P; Daviaud, D; Canivet, A; Grunenwald, S; Pienkowski, C; Chaumeil, J; Mejia, J E; Guery, J C TLR7 escapes X chromosome inactivation in immune cells Article de journal Sci Immunol, 3 (19), 2018, ISSN: 2470-9468 (Electronic) 2470-9468 (Linking), (In the top 5% of all research outputs scored by Altmetric. http://www.altmetric.com/details/32261033). @article{RN25b, title = {TLR7 escapes X chromosome inactivation in immune cells}, author = {Souyris, M. and Cenac, C. and Azar, P. and Daviaud, D. and Canivet, A. and Grunenwald, S. and Pienkowski, C. and Chaumeil, J. and Mejia, J. E. and Guery, J. C.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/29374079}, doi = {10.1126/sciimmunol.aap8855}, issn = {2470-9468 (Electronic) 2470-9468 (Linking)}, year = {2018}, date = {2018-01-26}, journal = {Sci Immunol}, volume = {3}, number = {19}, note = {In the top 5% of all research outputs scored by Altmetric. http://www.altmetric.com/details/32261033}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Eissmann, M F; Dijkstra, C; Wouters, M A; Baloyan, D; Mouradov, D; Nguyen, P M; Davalos-Salas, M; Putoczki, T L; Sieber, O M; Mariadason, J M; Ernst, M; Masson, F Interleukin 33 Signaling Restrains Sporadic Colon Cancer in an Interferon-gamma-Dependent Manner Article de journal Cancer Immunol Res, 6 (4), p. 409-421, 2018, ISSN: 2326-6074 (Electronic) 2326-6066 (Linking). @article{RN1b, title = {Interleukin 33 Signaling Restrains Sporadic Colon Cancer in an Interferon-gamma-Dependent Manner}, author = {Eissmann, M. F. and Dijkstra, C. and Wouters, M. A. and Baloyan, D. and Mouradov, D. and Nguyen, P. M. and Davalos-Salas, M. and Putoczki, T. L. and Sieber, O. M. and Mariadason, J. M. and Ernst, M. and Masson, F.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/29463593}, doi = {10.1158/2326-6066.CIR-17-0218}, issn = {2326-6074 (Electronic) 2326-6066 (Linking)}, year = {2018}, date = {2018-01-01}, journal = {Cancer Immunol Res}, volume = {6}, number = {4}, pages = {409-421}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Houmadi, R; Guipouy, D; Rey-Barroso, J; Vasconcelos, Z; Cornet, J; Manghi, M; Destainville, N; Valitutti, S; Allart, S; Dupre, L The Wiskott-Aldrich Syndrome Protein Contributes to the Assembly of the LFA-1 Nanocluster Belt at the Lytic Synapse Article de journal Cell Rep, 22 (4), p. 979-991, 2018, ISSN: 2211-1247 (Electronic). @article{RN3b, title = {The Wiskott-Aldrich Syndrome Protein Contributes to the Assembly of the LFA-1 Nanocluster Belt at the Lytic Synapse}, author = {Houmadi, R. and Guipouy, D. and Rey-Barroso, J. and Vasconcelos, Z. and Cornet, J. and Manghi, M. and Destainville, N. and Valitutti, S. and Allart, S. and Dupre, L.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/29386139}, doi = {10.1016/j.celrep.2017.12.088}, issn = {2211-1247 (Electronic)}, year = {2018}, date = {2018-01-01}, journal = {Cell Rep}, volume = {22}, number = {4}, pages = {979-991}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Gaud, G; Lesourne, R; Love, P E Regulatory mechanisms in T cell receptor signalling Article de journal Nat Rev Immunol, 2018, ISSN: 1474-1741 (Electronic) 1474-1733 (Linking). @article{RN1b, title = {Regulatory mechanisms in T cell receptor signalling}, author = {Gaud, G. and Lesourne, R. and Love, P. E.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/29789755}, doi = {10.1038/s41577-018-0020-8}, issn = {1474-1741 (Electronic) 1474-1733 (Linking)}, year = {2018}, date = {2018-01-01}, journal = {Nat Rev Immunol}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Betourne, A; Szelechowski, M; Thouard, A; Abrial, E; Jean, A; Zaidi, F; Foret, C; Bonnaud, E M; Charlier, C M; Suberbielle, E; Malnou, C E; Granon, S; Rampon, C; Gonzalez-Dunia, D Hippocampal expression of a virus-derived protein impairs memory in mice Article de journal Proc Natl Acad Sci U S A, 115 (7), p. 1611-1616, 2018, ISSN: 1091-6490 (Electronic) 0027-8424 (Linking). @article{RN108, title = {Hippocampal expression of a virus-derived protein impairs memory in mice}, author = {Betourne, A. and Szelechowski, M. and Thouard, A. and Abrial, E. and Jean, A. and Zaidi, F. and Foret, C. and Bonnaud, E. M. and Charlier, C. M. and Suberbielle, E. and Malnou, C. E. and Granon, S. and Rampon, C. and Gonzalez-Dunia, D.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/29378968}, doi = {10.1073/pnas.1711977115}, issn = {1091-6490 (Electronic) 0027-8424 (Linking)}, year = {2018}, date = {2018-01-01}, journal = {Proc Natl Acad Sci U S A}, volume = {115}, number = {7}, pages = {1611-1616}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Colin, P; Zhou, Z; Staropoli, I; Garcia-Perez, J; Gasser, R; Armani-Tourret, M; Benureau, Y; Gonzalez, N; Jin, J; Connell, B J; Raymond, S; Delobel, P; Izopet, J; Lortat-Jacob, H; Alcami, J; Arenzana-Seisdedos, F; Brelot, A; Lagane, B CCR5 structural plasticity shapes HIV-1 phenotypic properties Article de journal PLoS Pathog, 14 (12), p. e1007432, 2018, ISSN: 1553-7374 (Electronic) 1553-7366 (Linking). @article{RN859, title = {CCR5 structural plasticity shapes HIV-1 phenotypic properties}, author = {Colin, P. and Zhou, Z. and Staropoli, I. and Garcia-Perez, J. and Gasser, R. and Armani-Tourret, M. and Benureau, Y. and Gonzalez, N. and Jin, J. and Connell, B. J. and Raymond, S. and Delobel, P. and Izopet, J. and Lortat-Jacob, H. and Alcami, J. and Arenzana-Seisdedos, F. and Brelot, A. and Lagane, B.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/30521629}, doi = {10.1371/journal.ppat.1007432}, issn = {1553-7374 (Electronic) 1553-7366 (Linking)}, year = {2018}, date = {2018-01-01}, journal = {PLoS Pathog}, volume = {14}, number = {12}, pages = {e1007432}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
2017 |
Tauber, Maïthé; Boulanouar, Kader; Diene, Gwenaelle; Çabal-Berthoumieu, Sophie; Ehlinger, Virginie; Fichaux-Bourin, Pascale; Molinas, Catherine; Faye, Sandy; Valette, Marion; Pourrinet, Jeanne; Cessans, Catie; Viaux-Sauvelon, Sylvie; Bascoul, Céline; Guedeney, Antoine; Delhanty, Patric; Geenen, Vincent; Martens, Henri; Muscatelli, Françoise; Cohen, David; Consoli, Angèle; Payoux, Pierre; Arnaud, Catherine; Salles, Jean-Pierre The Use of Oxytocin to Improve Feeding and Social Skills in Infants With Prader–Willi Syndrome Article de journal PEDIATRICS, 139 (2), p. e2 0162976, 2017. @article{RN10b, title = {The Use of Oxytocin to Improve Feeding and Social Skills in Infants With Prader–Willi Syndrome}, author = {Maïthé Tauber and Kader Boulanouar and Gwenaelle Diene and Sophie Çabal-Berthoumieu and Virginie Ehlinger and Pascale Fichaux-Bourin and Catherine Molinas and Sandy Faye and Marion Valette and Jeanne Pourrinet and Catie Cessans and Sylvie Viaux-Sauvelon and Céline Bascoul and Antoine Guedeney and Patric Delhanty and Vincent Geenen and Henri Martens and Françoise Muscatelli and David Cohen and Angèle Consoli and Pierre Payoux and Catherine Arnaud and Salles, Jean-Pierre}, year = {2017}, date = {2017-01-01}, journal = {PEDIATRICS}, volume = {139}, number = {2}, pages = {e2 0162976}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Asrir, A; Aloulou, M; Gador, M; Perals, C; Fazilleau, N Interconnected subsets of memory follicular helper T cells have different effector functions Article de journal Nat Commun, 8 (1), p. 847, 2017, ISSN: 2041-1723 (Electronic) 2041-1723 (Linking). @article{RN2b, title = {Interconnected subsets of memory follicular helper T cells have different effector functions}, author = {Asrir, A. and Aloulou, M. and Gador, M. and Perals, C. and Fazilleau, N.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/29018187}, doi = {10.1038/s41467-017-00843-7}, issn = {2041-1723 (Electronic) 2041-1723 (Linking)}, year = {2017}, date = {2017-01-01}, journal = {Nat Commun}, volume = {8}, number = {1}, pages = {847}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Duguet, F; Locard-Paulet, M; Marcellin, M; Chaoui, K; Bernard, I; Andreoletti, O; Lesourne, R; Burlet-Schiltz, O; Gonzalez de Peredo, A; Saoudi, A Proteomic Analysis of Regulatory T Cells Reveals the Importance of Themis1 in the Control of Their Suppressive Function Article de journal Mol Cell Proteomics, 16 (8), p. 1416-1432, 2017, ISSN: 1535-9484 (Electronic) 1535-9476 (Linking). @article{RN4b, title = {Proteomic Analysis of Regulatory T Cells Reveals the Importance of Themis1 in the Control of Their Suppressive Function}, author = {Duguet, F. and Locard-Paulet, M. and Marcellin, M. and Chaoui, K. and Bernard, I. and Andreoletti, O. and Lesourne, R. and Burlet-Schiltz, O. and Gonzalez de Peredo, A. and Saoudi, A.}, url = {http://www.ncbi.nlm.nih.gov/pubmed/28373295}, doi = {10.1074/mcp.M116.062745}, issn = {1535-9484 (Electronic) 1535-9476 (Linking)}, year = {2017}, date = {2017-01-01}, journal = {Mol Cell Proteomics}, volume = {16}, number = {8}, pages = {1416-1432}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Laffont, Sophie; Blanquart, Eve; Savignac, Magali; Cenac, Claire; Laverny, Gilles; Metzger, Daniel; Girard, Jean-Philippe; Belz, Gabrielle T; Pelletier, Lucette; Seillet, Cyril; Guery, Jean-Charles Androgen signaling negatively controls group 2 innate lymphoid cells Article de journal J Exp Med, 214 (6), p. 1581-1592, 2017, ISSN: 1540-9538 (Electronic) 0022-1007 (Linking). @article{RN3, title = {Androgen signaling negatively controls group 2 innate lymphoid cells}, author = {Sophie Laffont and Eve Blanquart and Magali Savignac and Claire Cenac and Gilles Laverny and Daniel Metzger and Jean-Philippe Girard and Gabrielle T Belz and Lucette Pelletier and Cyril Seillet and Jean-Charles Guery}, url = {https://www.ncbi.nlm.nih.gov/pubmed/28484078}, doi = {10.1084/jem.20161807}, issn = {1540-9538 (Electronic) 0022-1007 (Linking)}, year = {2017}, date = {2017-01-01}, journal = {J Exp Med}, volume = {214}, number = {6}, pages = {1581-1592}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Yshii, L M; Hohlfeld, R; Liblau, R S Inflammatory CNS disease caused by immune checkpoint inhibitors: status and perspectives Article de journal Nat Rev Neurol, 13 (12), p. 755-763, 2017, ISSN: 1759-4766 (Electronic) 1759-4758 (Linking). @article{RN5b, title = {Inflammatory CNS disease caused by immune checkpoint inhibitors: status and perspectives}, author = {Yshii, L. M. and Hohlfeld, R. and Liblau, R. S.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/29104289}, doi = {10.1038/nrneurol.2017.144}, issn = {1759-4766 (Electronic) 1759-4758 (Linking)}, year = {2017}, date = {2017-01-01}, journal = {Nat Rev Neurol}, volume = {13}, number = {12}, pages = {755-763}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Joulia, R; Mailhol, C; Valitutti, S; Didier, A; Espinosa, E Direct monitoring of basophil degranulation by using avidin-based probes Article de journal J Allergy Clin Immunol, 2017, ISSN: 1097-6825 (Electronic) 0091-6749 (Linking). @article{RN16, title = {Direct monitoring of basophil degranulation by using avidin-based probes}, author = {Joulia, R. and Mailhol, C. and Valitutti, S. and Didier, A. and Espinosa, E.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/28433691}, doi = {10.1016/j.jaci.2017.03.030}, issn = {1097-6825 (Electronic) 0091-6749 (Linking)}, year = {2017}, date = {2017-01-01}, journal = {J Allergy Clin Immunol}, keywords = {}, pubstate = {published}, tppubtype = {article} } |