@article{Pichler2023,

title = {TCR-independent CD137 (4-1BB) signaling promotes CD8+-exhausted T cell proliferation and terminal differentiation},

author = {Pichler, Andrea; Carrie, Nadege; Cuisinier, Marine; Ghazali, Samira; Voisin, Alison; Axisa, Pierre-Paul; Tosolini, Marie; Mazzotti, Céline; Golec, Dominic; Maheo, Sabrina; Souto, Laura; Ekren, Ruchan; Blanquart, Eve; Lemaitre, Lea; Feliu, Virginie; Joubert, Marie-Véronique; Cannons, Jennifer; Guillerey, Camille; Avet-Loiseau, Herve; Watts, Tania; Salomon, Benoit; Joffre, Olivier; Grinberg-Bleyer, Yenkel; Schwarzberg, Pamela; Lucca, Liliana; Martinet, Ludovic},

editor = {Cell Press},

year  = {2023},

date = {2023-06-30},

journal = {Immunity},

volume = {56},

pages = {1-18},

abstract = {CD137 (4-1BB)-activating receptor represents a promising cancer immunotherapeutic target. Yet, the cellular program driven by CD137 and its role in cancer immune surveillance remain unresolved. Using T cell-specific deletion and agonist antibodies, we found that CD137 modulates tumor infiltration of CD8+-exhausted T (Tex) cells expressing PD1, Lag-3, and Tim-3 inhibitory receptors. T cell-intrinsic, TCR-independent CD137 signaling stimulated the proliferation and the terminal differentiation of Tex precursor cells through a mechanism involving the RelA and cRel canonical NF-κB subunits and Tox-dependent chromatin remodeling. While Tex cell accumulation induced by prophylactic CD137 agonists favored tumor growth, anti-PD1 efficacy was improved with subsequent CD137 stimulation in pre-clinical mouse models. Better understanding of T cell exhaustion has crucial implications for the treatment of cancer and infectious diseases. Our results identify CD137 as a critical regulator of Tex cell expansion and differentiation that holds potential for broad therapeutic applications.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Scholaert†2023,

title = {3D deconvolution of human skin immune architecture with Multiplex Annotated Tissue Imaging System},

author = {Manon Scholaert† and Raissa Houmadi† and Jeremy Martin† and Nadine Serhan† and Marie Tauber and Emilie Braun and Lilian Basso and Eric Merle and Pascal Descargues and Manuelle Viguier and Cécile Lesort and Benoît Chaput and Jean Kanitakis and Denis Jullien and Cristina Bulai Livideanu and Laurence Lamant and Emeline Pagès and Nicolas Gaudenzio},

url = {https://www-science-org.proxy.insermbiblio.inist.fr/doi/10.1126/sciadv.adf9491},

doi = {10.1126/sciadv.adf9491},

year  = {2023},

date = {2023-06-07},

journal = {Science Advances},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{block_systemic_2023,

title = {Systemic Inflammation and Normocytic Anemia in DOCK11 Deficiency},

author = {Block, Jana and Rashkova, Christina and Castanon, Irinka and Zoghi, Samaneh and Platon, Jessica and Ardy, Rico C. and Fujiwara, Mitsuhiro and Chaves, Beatriz and Schoppmeyer, Rouven and van der Made, Caspar I. and Jimenez Heredia, Raul and Harms, Frederike L. and Alavi, Samin and Alsina, Laia and Sanchez Moreno, Paula and Ávila Polo, Rainiero and Cabrera-Pérez, Rocío and Kostel Bal, Sevgi and Pfajfer, Laurène and Ransmayr, Bernhard and Mautner, Anna-Katharina and Kondo, Ryohei and Tinnacher, Anna and Caldera, Michael and Schuster, Michael and Domínguez Conde, Cecilia and Platzer, René and Salzer, Elisabeth and Boyer, Thomas and Brunner, Han G. and Nooitgedagt-Frons, Judith E. and Iglesias, Estíbaliz and Deyà-Martinez, Angela and Camacho-Lovillo, Marisol and Menche, Jörg and Bock, Christoph and Huppa, Johannes B. and Pickl, Winfried F. and Distel, Martin and Yoder, Jeffrey A. and Traver, David and Engelhardt, Karin R. and Linden, Tobias and Kager, Leo and Hannich, J. Thomas and Hoischen, Alexander and Hambleton, Sophie and Illsinger, Sabine and Da Costa, Lydie and Kutsche, Kerstin and Chavoshzadeh, Zahra and van Buul, Jaap D. and Antón, Jordi and Calzada-Hernández, Joan and Neth, Olaf and Viaud, Julien and Nishikimi, Akihiko and Dupré, Loïc and Boztug, Kaan},

doi = {10.1056/NEJMoa2210054},

issn = {1533-4406},

year  = {2023},

date = {2023-06-01},

journal = {N Engl J Med},

abstract = {BACKGROUND: Increasing evidence links genetic defects affecting actin-regulatory proteins to diseases with severe autoimmunity and autoinflammation, yet the underlying molecular mechanisms are poorly understood. Dedicator of cytokinesis 11 (DOCK11) activates the small Rho guanosine triphosphatase (GTPase) cell division cycle 42 (CDC42), a central regulator of actin cytoskeleton dynamics. The role of DOCK11 in human immune-cell function and disease remains unknown. 

METHODS: We conducted genetic, immunologic, and molecular assays in four patients from four unrelated families who presented with infections, early-onset severe immune dysregulation, normocytic anemia of variable severity associated with anisopoikilocytosis, and developmental delay. Functional assays were performed in patient-derived cells, as well as in mouse and zebrafish models. 

RESULTS: We identified rare, X-linked germline mutations in DOCK11 in the patients, leading to a loss of protein expression in two patients and impaired CDC42 activation in all four patients. Patient-derived T cells did not form filopodia and showed abnormal migration. In addition, the patient-derived T cells, as well as the T cells from Dock11-knockout mice, showed overt activation and production of proinflammatory cytokines that were associated with an increased degree of nuclear translocation of nuclear factor of activated T cell 1 (NFATc1). Anemia and aberrant erythrocyte morphologic features were recapitulated in a newly generated dock11-knockout zebrafish model, and anemia was amenable to rescue on ectopic expression of constitutively active CDC42. 

CONCLUSIONS: Germline hemizygous loss-of-function mutations affecting the actin regulator DOCK11 were shown to cause a previously unknown inborn error of hematopoiesis and immunity characterized by severe immune dysregulation and systemic inflammation, recurrent infections, and anemia. (Funded by the European Research Council and others.).},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Defaye2023,

title = {The neuronal tyrosine kinase receptor ligand ALKAL2 mediates persistent pain},

author = {Manon Defaye and Mircea C. Iftinca and Vinicius M. Gadotti and Lilian Basso and Nasser S. Abdullah and Mélissa Cuménal and Francina Agosti and Ahmed Hassan and Robyn Flynn and Jérémy Martin and Vanessa Soubeyre and Gaetan Poulen and Nicolas Lonjon and Florence Vachiery-Lahaye and Luc Bauchet and Pierre Francois Mery and Emmanuel Bourinet and Gerald W. Zamponi and Christophe Altier},

url = {https://www-jci-org.proxy.insermbiblio.inist.fr/articles/view/154317},

doi = {https://doi.org/10.1172/JCI154317},

year  = {2023},

date = {2023-05-24},

journal = {The Journal of Clinical Investigation},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid37126681,

title = {Epigenetic silencing of selected hypothalamic neuropeptides in narcolepsy with cataplexy},

author = {Ali Seifinejad and Mergim Ramosaj and Ling Shan and Sha Li and Marie-Laure Possovre and Corinne Pfister and Rolf Fronczek and Lee A Garrett-Sinha and David Frieser and Makoto Honda and Yoan Arribat and Dogan Grepper and Francesca Amati and Marie Picot and Andrea Agnoletto and Christian Iseli and Nicolas Chartrel and Roland Liblau and Gert J Lammers and Anne Vassalli and Mehdi Tafti},

doi = {10.1073/pnas.2220911120},

issn = {1091-6490},

year  = {2023},

date = {2023-05-01},

urldate = {2023-05-01},

journal = {Proc Natl Acad Sci U S A},

volume = {120},

number = {19},

pages = {e2220911120},

abstract = {Narcolepsy with cataplexy is a sleep disorder caused by deficiency in the hypothalamic neuropeptide hypocretin/orexin (HCRT), unanimously believed to result from autoimmune destruction of hypocretin-producing neurons. HCRT deficiency can also occur in secondary forms of narcolepsy and be only temporary, suggesting it can occur without irreversible neuronal loss. The recent discovery that narcolepsy patients also show loss of hypothalamic (corticotropin-releasing hormone) CRH-producing neurons suggests that other mechanisms than cell-specific autoimmune attack, are involved. Here, we identify the HCRT cell-colocalized neuropeptide QRFP as the best marker of HCRT neurons. We show that if HCRT neurons are ablated in mice, in addition to   transcript is also lost in the lateral hypothalamus, while in mice where only the  gene is inactivated  is unchanged. Similarly, postmortem hypothalamic tissues of narcolepsy patients show preserved  expression, suggesting the neurons are present but fail to actively produce HCRT. We show that the promoter of the  gene of patients exhibits hypermethylation at a methylation-sensitive and evolutionary-conserved PAX5:ETS1 transcription factor-binding site, suggesting the gene is subject to transcriptional silencing. We show also that in addition to HCRT,  and Dynorphin () gene promoters, exhibit hypermethylation in the hypothalamus of patients. Altogether, we propose that , , and  are epigenetically silenced by a hypothalamic assault (inflammation) in narcolepsy patients, without concurrent cell death. Since methylation is reversible, our findings open the prospect of reversing or curing narcolepsy.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid37253744,

title = {Antigen recognition detains CD8 T cells at the blood-brain barrier and contributes to its breakdown},

author = {Sidar Aydin and Javier Pareja and Vivianne M Schallenberg and Armelle Klopstein and Thomas Gruber and Nicolas Page and Elisa Bouillet and Nicolas Blanchard and Roland Liblau and Jakob Körbelin and Markus Schwaninger and Aaron J Johnson and Mirjam Schenk and Urban Deutsch and Doron Merkler and Britta Engelhardt},

doi = {10.1038/s41467-023-38703-2},

issn = {2041-1723},

year  = {2023},

date = {2023-05-01},

urldate = {2023-05-01},

journal = {Nat Commun},

volume = {14},

number = {1},

pages = {3106},

abstract = {Blood-brain barrier (BBB) breakdown and immune cell infiltration into the central nervous system (CNS) are early hallmarks of multiple sclerosis (MS). High numbers of CD8 T cells are found in MS lesions, and antigen (Ag) presentation at the BBB has been proposed to promote CD8 T cell entry into the CNS. Here, we show that brain endothelial cells process and cross-present Ag, leading to effector CD8 T cell differentiation. Under physiological flow in vitro, endothelial Ag presentation prevented CD8 T cell crawling and diapedesis resulting in brain endothelial cell apoptosis and BBB breakdown. Brain endothelial Ag presentation in vivo was limited due to Ag uptake by CNS-resident macrophages but still reduced motility of Ag-specific CD8 T cells within CNS microvessels. MHC class I-restricted Ag presentation at the BBB during neuroinflammation thus prohibits CD8 T cell entry into the CNS and triggers CD8 T cell-mediated focal BBB breakdown.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{36883943,

title = {Parasitic Infections and Biological Therapies Targeting Type 2 Inflammation: A VigiBase Study},

author = {Lifar P and Montastruc F and Reber LL and Magnaval JF and Guilleminault L},

url = {https://pubmed.ncbi.nlm.nih.gov/36883943/},

doi = { 10.1164/rccm.202210-1898LE},

year  = {2023},

date = {2023-05-01},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{37022292,

title = {Conditional neutrophil depletion challenges their contribution to mouse models of anaphylaxis.},

author = {Stackowicz J and Gillis CM and Godon O and Iannascoli B and Conde E and Leveque E and Worrall WPM and Galli SJ and Bruhns P and Reber LL and Jönsson F},

url = {https://pubmed.ncbi.nlm.nih.gov/37022292/},

doi = {10.1111/all.15738},

year  = {2023},

date = {2023-04-06},

journal = {Allergy},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid36586513,

title = {Time to negative PCR conversion amongst high-risk patients with mild-to-moderate Omicron BA.1 and BA.2 COVID-19 treated with sotrovimab or nirmatrelvir},

author = {Guillaume Martin-Blondel and Anne-Geneviève Marcelin and Cathia Soulié and Sofia Kaisaridi and Clovis Lusivika-Nzinga and Karen Zafilaza and Céline Dorival and Laura Nailler and Anaïs Boston and Anne-Marie Ronchetti and Cléa Melenotte and André Cabié and Christophe Choquet and Albert Trinh-Duc and Karine Lacombe and Géraldine Gaube and François Coustillères and Valérie Pourcher and Jean-Philippe Martellosio and Nathan Peiffer-Smadja and Marie Chauveau and Pierre Housset and Lionel Piroth and Mathilde Devaux and Gilles Pialoux and Aurélie Martin and Vincent Dubee and Jérôme Frey and Audrey Le Bot and Charles Cazanave and Philippe Petua and Roland Liblau and Fabrice Carrat and Youri Yordanov},

doi = {10.1016/j.cmi.2022.12.016},

issn = {1469-0691},

year  = {2023},

date = {2023-04-01},

urldate = {2023-04-01},

journal = {Clin Microbiol Infect},

volume = {29},

number = {4},

pages = {543.e5--543.e9},

abstract = {OBJECTIVES: Our aim was to compare the clinical and virological outcomes in Omicron BA.1- and BA.2-infected patients who received sotrovimab with those in patients who received nirmatrelvir for the prevention of severe COVID-19.nnMETHODS: In this multi-centric, prospective ANRS 0003S CoCoPrev cohort study, patients at a high risk of progression of mild-to-moderate BA.1 or BA.2 COVID-19 who received sotrovimab or nirmatrelvir were included. The proportion of patients with progression to severe COVID-19, time between the start of treatment to negative PCR conversion, SARS-CoV-2 viral decay, and characterization of resistance variants were determined. A multi-variable Cox proportional hazard model was used to determine the time to negative PCR conversion and a mixed-effect model for the dynamics of viral decay.nnRESULTS: Amongst 255 included patients, 199 (80%) received ≥3 vaccine doses, 195 (76%) received sotrovimab, and 60 (24%) received nirmatrelvir. On day 28, new COVID-19-related hospitalization occurred in 4 of 193 (2%; 95% CI, 1-5%) sotrovimab-treated patients and 0 of 55 nirmatrelvir-treated patients (p 0.24). One out of the 55 nirmatrelvir-treated patients died (2%; 95% CI, 0-10%). The median time to negative PCR conversion was 11.5 days (95% CI, 10.5-13) in the sotrovimab-treated patients vs. 4 days (95% CI, 4-9) in the nirmatrelvir-treated patients (p < 0.001). Viral decay was faster in the patients who received nirmatrelvir (p < 0.001). In the multi-variable analysis, nirmatrelvir and nasopharyngeal PCR cycle threshold values were independently associated with faster conversion to negative PCR (hazard ratio, 2.35; 95% CI, 1.56-3.56; p < 0.0001 and hazard ratio, 1.05; 95% CI, 1.01-1.08; p 0.01, respectively).nnCONCLUSIONS: Early administration of nirmatrelvir in high-risk patients compared with that of sotrovimab was associated with faster viral clearance. This may participate to decrease transmission and prevent viral resistance.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{36799426,

title = {A vaccine targeting human IL-4 and IL-13 protects against asthma in humanized mice.},

author = {Lamanna E and Conde E and Mougel A and Bonnefoy J and Colaone F and Godon O and Hamdi S and Kamphuis JBJ and Drouet B and Serra V and Bruhns P and Reber LL},

url = {https://pubmed.ncbi.nlm.nih.gov/36799426/},

doi = {10.1111/all.15680},

year  = {2023},

date = {2023-02-17},

journal = {Allergy},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid36729270,

title = {A Pilot Study to Develop Paraneoplastic Cerebellar Degeneration Mouse Model},

author = {Fabrice Faure and Lidia Yshii and Toufic Renno and Isabelle Coste and Bastien Joubert and Virginie Desestret and Roland Liblau and Jérôme Honnorat},

doi = {10.1007/s12311-023-01524-6},

issn = {1473-4230},

year  = {2023},

date = {2023-02-01},

urldate = {2023-02-01},

journal = {Cerebellum},

abstract = {Modeling paraneoplastic neurological diseases to understand the immune mechanisms leading to neuronal death is a major challenge given the rarity and terminal access of patients' autopsies. Here, we present a pilot study aiming at modeling paraneoplastic cerebellar degeneration with Yo autoantibodies (Yo-PCD). Female mice were implanted with an ovarian carcinoma cell line expressing CDR2 and CDR2L, the known antigens recognized by anti-Yo antibodies. To boost the immune response, we also immunized the mice by injecting antigens with diverse adjuvants and immune checkpoint inhibitors. Ataxia and gait instability were assessed in treated mice as well as autoantibody levels, Purkinje cell density, and immune infiltration in the cerebellum. We observed the production of anti-Yo antibodies in the CSF and serum of all immunized mice. Brain immunoreaction varied depending on the site of implantation of the tumor, with subcutaneous administration leading to a massive infiltration of immune cells in the meningeal spaces, choroid plexus, and cerebellar parenchyma. However, we did not observe massive Purkinje cell death nor any motor impairments in any of the experimental groups. Self-sustained neuro-inflammation might require a longer time to build up in our model. Unusual tumor antigen presentation and/or intrinsic, species-specific factors required for pro-inflammatory engagement in the brain may also constitute strong limitations to achieve massive recruitment of antigen-specific T-cells and killing of antigen-expressing neurons in this mouse model.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid35900406c,

title = {Mortalin/Hspa9 involvement and therapeutic perspective in Parkinson's disease},

author = {Baptiste Texier and Morgane Prime and Djamaa Atamena and Pascale Belenguer and Marion Szelechowski},

doi = {10.4103/1673-5374.346487},

issn = {1673-5374},

year  = {2023},

date = {2023-02-01},

urldate = {2023-02-01},

journal = {Neural Regen Res},

volume = {18},

number = {2},

pages = {293--298},

abstract = {By controlling the proper folding of proteins imported into mitochondria and ensuring crosstalk between the reticulum and mitochondria to modulate intracellular calcium fluxes, Mortalin is a chaperone protein that plays crucial roles in neuronal homeostasis and activity. However, its expression and stability are strongly modified in response to cellular stresses, in particular upon altered oxidative conditions during neurodegeneration. Here, we report and discuss the abundant literature that has highlighted its contribution to the pathophysiology of Parkinson's disease, as well as its therapeutic and prognostic potential in this still incurable pathology.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid35900406b,

title = {Mortalin/Hspa9 involvement and therapeutic perspective in Parkinson's disease},

author = {Baptiste Texier and Morgane Prime and Djamaa Atamena and Pascale Belenguer and Marion Szelechowski},

doi = {10.4103/1673-5374.346487},

issn = {1673-5374},

year  = {2023},

date = {2023-02-01},

journal = {Neural Regen Res},

volume = {18},

number = {2},

pages = {293--298},

abstract = {By controlling the proper folding of proteins imported into mitochondria and ensuring crosstalk between the reticulum and mitochondria to modulate intracellular calcium fluxes, Mortalin is a chaperone protein that plays crucial roles in neuronal homeostasis and activity. However, its expression and stability are strongly modified in response to cellular stresses, in particular upon altered oxidative conditions during neurodegeneration. Here, we report and discuss the abundant literature that has highlighted its contribution to the pathophysiology of Parkinson's disease, as well as its therapeutic and prognostic potential in this still incurable pathology.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid35900406,

title = {Mortalin/Hspa9 involvement and therapeutic perspective in Parkinson's disease},

author = {Baptiste Texier and Morgane Prime and Djamaa Atamena and Pascale Belenguer and Marion Szelechowski},

doi = {10.4103/1673-5374.346487},

issn = {1673-5374},

year  = {2023},

date = {2023-02-01},

journal = {Neural Regen Res},

volume = {18},

number = {2},

pages = {293--298},

abstract = {By controlling the proper folding of proteins imported into mitochondria and ensuring crosstalk between the reticulum and mitochondria to modulate intracellular calcium fluxes, Mortalin is a chaperone protein that plays crucial roles in neuronal homeostasis and activity. However, its expression and stability are strongly modified in response to cellular stresses, in particular upon altered oxidative conditions during neurodegeneration. Here, we report and discuss the abundant literature that has highlighted its contribution to the pathophysiology of Parkinson's disease, as well as its therapeutic and prognostic potential in this still incurable pathology.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Fourgeaud2023,

title = {Clinical Value of Serial Quantitative Analysis of Cytomegalovirus DNA in Blood and Saliva Over the First 24 Months of Life in Congenital Infection: The French Cymepedia Cohort},

author = {Jacques Fourgeaud and Jean-François Magny and Sophie Couderc and Patricia Garcia and Anne-Marie Maillotte and Melinda Benard and Didier Pinquier and Philippe Minodier and Dominique Astruc and Hugues Patural and Melissa Ugolin and Sophie Parat and Bernard Guillois and Armelle Garenne and Tiffany Guilleminot and Marine Parodi and Laurence Bussières and Yves Ville and Marianne Leruez-Ville},

doi = {10.1016/j.jpeds.2022.09.040},

issn = {0022-3476},

year  = {2023},

date = {2023-02-00},

urldate = {2023-02-00},

journal = {The Journal of Pediatrics},

volume = {253},

pages = {197--204.e5},

publisher = {Elsevier BV},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Starkl2023,

title = {Pre-print | Mast cell-derived BH4 is a critical mediator of postoperative pain},

author = {Philipp Starkl and Gustav Jonsson and Tyler Artner and Bruna Lenfers Turnes and Nadine Serhan and Tiago Oliveira and Laura-Marie Gail and Karel Stejskal and Keith M. Channon and Thomas Köcher and Georg Stary and Victoria Klang and Nicolas Gaudenzio and Sylvia Knapp and Clifford J. Woolf and Josef M. Penninger and Shane J.F. Cronin},

url = {https://www.biorxiv.org/content/10.1101/2023.01.24.525378v1},

year  = {2023},

date = {2023-01-24},

journal = {bioRxiv},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN2124,

title = {Characteristics of the (Auto)Reactive T Cells in Rheumatoid Arthritis According to the Immune Epitope Database},

author = {C. Carle and Y. Degboe and A. Ruyssen-Witrand and M. I. Arleevskaya and C. Clavel and Y. Renaudineau},

url = {https://www.ncbi.nlm.nih.gov/pubmed/36901730},

doi = {10.3390/ijms24054296},

issn = {1422-0067 (Electronic) 1422-0067 (Linking)},

year  = {2023},

date = {2023-01-01},

urldate = {2023-01-01},

journal = {Int J Mol Sci},

volume = {24},

number = {5},

abstract = {T cells are known to be involved in the pathogenesis of rheumatoid arthritis (RA). Accordingly, and to better understand T cells' contribution to RA, a comprehensive review based on an analysis of the Immune Epitope Database (IEDB) was conducted. An immune CD8+ T cell senescence response is reported in RA and inflammatory diseases, which is driven by active viral antigens from latent viruses and cryptic self-apoptotic peptides. RA-associated pro-inflammatory CD4+ T cells are selected by MHC class II and immunodominant peptides, which are derived from molecular chaperones, host extra-cellular and cellular peptides that could be post-translationally modified (PTM), and bacterial cross-reactive peptides. A large panel of techniques have been used to characterize (auto)reactive T cells and RA-associated peptides with regards to their interaction with the MHC and TCR, capacity to enter the docking site of the shared epitope (DRB1-SE), capacity to induce T cell proliferation, capacity to select T cell subsets (Th1/Th17, Treg), and clinical contribution. Among docking DRB1-SE peptides, those with PTM expand autoreactive and high-affinity CD4+ memory T cells in RA patients with an active disease. Considering original therapeutic options in RA, mutated, or altered peptide ligands (APL) have been developed and are tested in clinical trials.},

note = {Carle, Caroline 

Degboe, Yannick 

Ruyssen-Witrand, Adeline 

Arleevskaya, Marina I 

Clavel, Cyril 

Renaudineau, Yves 

eng 

2023/Societe Francaise de Rhumatologie/ 

17-15-01099/Russian Science Foundation/ 

Review 

Switzerland 

2023/03/12 

Int J Mol Sci. 2023 Feb 21;24(5):4296. doi: 10.3390/ijms24054296.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid37033984,

title = {Anti-CD20 therapies in multiple sclerosis: From pathology to the clinic},

author = {Jérôme de Sèze and Elisabeth Maillart and Antoine Gueguen and David A Laplaud and Laure Michel and Eric Thouvenot and Hélène Zephir and Luc Zimmer and Damien Biotti and Roland Liblau},

doi = {10.3389/fimmu.2023.1004795},

issn = {1664-3224},

year  = {2023},

date = {2023-01-01},

urldate = {2023-01-01},

journal = {Front Immunol},

volume = {14},

pages = {1004795},

abstract = {The immune system plays a significant role in multiple sclerosis. While MS was historically thought to be T cell-mediated, multiple pieces of evidence now support the view that B cells are essential players in multiple sclerosis pathogenic processes. High-efficacy disease-modifying therapies that target the immune system have emerged over the past two decades. Anti-CD20 monoclonal antibodies selectively deplete CD20+ B and CD20+ T cells and efficiently suppress inflammatory disease activity. These monotherapies prevent relapses, reduce new or active magnetic resonance imaging brain lesions, and lessen disability progression in patients with relapsing multiple sclerosis. Rituximab, ocrelizumab, and ofatumumab are currently used in clinical practice, while phase III clinical trials for ublituximab have been recently completed. In this review, we compare the four anti-CD20 antibodies in terms of their mechanisms of action, routes of administration, immunological targets, and pharmacokinetic properties. A deeper understanding of the individual properties of these molecules in relation to their efficacy and safety profiles is critical for their use in clinical practice.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid37122721,

title = {Cerebrospinal fluid proteomics in recent-onset Narcolepsy type 1 reveals activation of the complement system},

author = {Ikram Ayoub and Yves Dauvilliers and Lucie Barateau and Thaïs Vermeulen and Emmanuelle Mouton-Barbosa and Marlène Marcellin and Anne Gonzalez-de-Peredo and Catharina C Gross and Abdelhadi Saoudi and Roland Liblau},

doi = {10.3389/fimmu.2023.1108682},

issn = {1664-3224},

year  = {2023},

date = {2023-01-01},

urldate = {2023-01-01},

journal = {Front Immunol},

volume = {14},

pages = {1108682},

abstract = {INTRODUCTION: Narcolepsy type 1 (NT1) is a rare, chronic and disabling neurological disease causing excessive daytime sleepiness and cataplexy. NT1 is characterized pathologically by an almost complete loss of neurons producing the orexin neuropeptides in the lateral hypothalamus. Genetic and environmental factors strongly suggest the involvement of the immune system in the loss of orexin neurons. The cerebrospinal fluid (CSF), secreted locally and surrounding the central nervous system (CNS), represents an accessible window into CNS pathological processes.nnMETHODS: To gain insight into the biological and molecular changes in NT1 patients, we performed a comparative proteomics analysis of the CSF from 21 recent-onset NT1 patients and from two control groups: group 1 with somatoform disorders, and group 2 patients with hypersomnia other than NT1, to control for any potential effect of sleep disturbances on CSF composition. To achieve an optimal proteomic coverage analysis, the twelve most abundant CSF proteins were depleted, and samples were analyzed by nano-flow liquid chromatography tandem mass spectrometry (nano-LC-MS/MS) using the latest generation of hybrid Orbitrap mass spectrometer.nnRESULTS AND DISCUSSION: Our study allowed the identification and quantification of up to 1943 proteins, providing a remarkably deep analysis of the CSF proteome. Interestingly, gene set enrichment analysis indicated that the complement and coagulation systems were enriched and significantly activated in NT1 patients in both cohorts analyzed. Notably, the lectin and alternative complement pathway as well as the downstream lytic membrane attack complex were congruently increased in NT1. Our data suggest that the complement dysregulation in NT1 patients can contribute to immunopathology either by directly promoting tissue damage or as part of local inflammatory responses. We therefore reveal an altered composition of the CSF proteome in NT1 patients, which points to an ongoing inflammatory process contributed, at least in part, by the complement system.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid36865563,

title = {Editorial: Dysregulation of Th17 and Treg cells in autoimmune diseases},

author = {Anne L Astier and David M Kofler},

doi = {10.3389/fimmu.2023.1151836},

issn = {1664-3224},

year  = {2023},

date = {2023-01-01},

urldate = {2023-01-01},

journal = {Front Immunol},

volume = {14},

pages = {1151836},

keywords = {},

pubstate = {published},

tppubtype = {article}

}