@article{pmid38713628,

title = {THEMIS promotes T cell development and maintenance by rising the signaling threshold of the inhibitory receptor BTLA},

author = {Suzanne Mélique and Aurélie Vadel and Nelly Rouquié and Cui Yang and Cyrielle Bories and Coline Cotineau and Abdelhadi Saoudi and Nicolas Fazilleau and Renaud Lesourne},

doi = {10.1073/pnas.2318773121},

issn = {1091-6490},

year  = {2024},

date = {2024-05-01},

urldate = {2024-05-01},

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

volume = {121},

number = {20},

pages = {e2318773121},

abstract = {The current paradigm about the function of T cell immune checkpoints is that these receptors switch on inhibitory signals upon cognate ligand interaction. We here revisit this simple switch model and provide evidence that the T cell lineage protein THEMIS enhances the signaling threshold at which the immune checkpoint BTLA (B- and T-lymphocyte attenuator) represses T cell responses. THEMIS is recruited to the cytoplasmic domain of BTLA and blocks its signaling capacity by promoting/stabilizing the oxidation of the catalytic cysteine of the tyrosine phosphatase SHP-1. In contrast, THEMIS has no detectable effect on signaling pathways regulated by PD-1 (Programmed cell death protein 1), which depend mainly on the tyrosine phosphatase SHP-2. BTLA inhibitory signaling is tuned according to the THEMIS expression level, making CD8+ T cells more resistant to BTLA-mediated inhibition than CD4+ T cells. In the absence of THEMIS, the signaling capacity of BTLA is exacerbated, which results in the attenuation of signals driven by the T cell antigen receptor and by receptors for IL-2 and IL-15, consequently hampering thymocyte positive selection and peripheral CD8+ T cell maintenance. By characterizing the pivotal role of THEMIS in restricting the transmission of BTLA signals, our study suggests that immune checkpoint operability is conditioned by intracellular signal attenuators.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Santamaria2024,

title = {The type 1 diabetes susceptibility locus Idd5 favours robust neonatal development of highly autoreactive regulatory T cells in the NOD mouse},

author = {Jérémy C. Santamaria and Sylvia Vuillier and Ariel O. Galindo-Albarrán and Sarah Castan and Claire Detraves and Olivier P. Joffre and Paola Romagnoli and Joost P. M. van Meerwijk},

doi = {10.3389/fimmu.2024.1358459},

issn = {1664-3224},

year  = {2024},

date = {2024-02-09},

journal = {Front. Immunol.},

volume = {15},

publisher = {Frontiers Media SA},

abstract = {Regulatory T lymphocytes expressing the transcription factor Foxp3 (Tregs) play an important role in the prevention of autoimmune diseases and other immunopathologies. Aberrations in Treg-mediated immunosuppression are therefore thought to be involved in the development of autoimmune pathologies, but few have been documented. Recent reports indicated a central role for Tregs developing during the neonatal period in the prevention of autoimmune pathology. We therefore investigated the development of Tregs in neonatal NOD mice, an important animal model for autoimmune type 1 diabetes. Surprisingly, we found that, as compared with seven other commonly studied inbred mouse strains, in neonatal NOD mice, exceptionally large proportions of developing Tregs express high levels of GITR and PD-1. The latter phenotype was previously associated with high Treg autoreactivity in C57BL/6 mice, which we here confirm for NOD animals. The proportions of newly developing GITRhighPD-1+ Tregs rapidly drop during the first week of age. A genome-wide genetic screen indicated the involvement of several diabetes susceptibility loci in this trait. Analysis of a congenic mouse strain confirmed that Idd5 contributes to the genetic control of GITRhighPD-1+ Treg development in neonates. Our data thus demonstrate an intriguing and paradoxical correlation between an idiosyncrasy in Treg development in NOD mice and their susceptibility to type 1 diabetes.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Joulia2024,

title = {Eomes-dependent mitochondrial regulation promotes survival of pathogenic CD4+ T cells during inflammation},

author = {Emeline Joulia and Michaël F. Michieletto and Arantxa Agesta and Cindy Peillex and Virginie Girault and Anne-Louise Le Dorze and Romain Peroceschi and Florence Bucciarelli and Marion Szelechowski and Adeline Chaubet and Nawad Hakim and Rémi Marrocco and Emeline Lhuillier and Manuel Lebeurrier and Rafael J. Argüello and Abdelhadi Saoudi and Hicham El Costa and Veronique Adoue and Thierry Walzer and Jean-Emmanuel Sarry and Anne S. Dejean},

doi = {10.1084/jem.20230449},

issn = {1540-9538},

year  = {2024},

date = {2024-02-05},

volume = {221},

number = {2},

publisher = {Rockefeller University Press},

abstract = {The mechanisms whereby Eomes controls tissue accumulation of T cells and strengthens inflammation remain ill-defined. Here, we show that Eomes deletion in antigen-specific CD4+ T cells is sufficient to protect against central nervous system (CNS) inflammation. While Eomes is dispensable for the initial priming of CD4+ T cells, it is required for long-term maintenance of CNS-infiltrating CD4+ T cells. We reveal that the impact of Eomes on effector CD4+ T cell longevity is associated with sustained expression of multiple genes involved in mitochondrial organization and functions. Accordingly, epigenetic studies demonstrate that Eomes supports mitochondrial function by direct binding to either metabolism-associated genes or mitochondrial transcriptional modulators. Besides, the significance of these findings was confirmed in CD4+ T cells from healthy donors and multiple sclerosis patients. Together, our data reveal a new mechanism by which Eomes promotes severity and chronicity of inflammation via the enhancement of CD4+ T cell mitochondrial functions and resistance to stress-induced cell death.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38424741,

title = {Increased levels of circulating soluble CD226 in multiple sclerosis},

author = {Saniya Kari and Florence Bucciarelli and Thibault Angles and Anne-Cecile Oster and Pauline Cauboue and Karl Laviolette and Madeline Mougenot and Elena Morandi and Isabelle Bernard and Beatrice Pignolet and Chloé Bost and Joelle Thomas and Leonor Nogueira and Abdelhadi Saoudi and Roland Liblau and Anne L Astier},

doi = {10.1177/13524585241234489},

issn = {1477-0970},

year  = {2024},

date = {2024-02-01},

urldate = {2024-02-01},

journal = {Mult Scler},

pages = {13524585241234489},

abstract = {BACKGROUND: The glycoprotein CD226 plays a key role in regulating immune cell function. Soluble CD226 (sCD226) is increased in sera of patients with several chronic inflammatory diseases but its levels in neuroinflammatory diseases such as multiple sclerosis (MS) are unknown.nnOBJECTIVE: To investigate the presence and functional implications of sCD226 in persons with multiple sclerosis (pwMS) and other neurological diseases.nnMETHODS: The mechanisms of sCD226 production were first investigated by analyzing CD226 surface expression levels and supernatants of CD3/CD226-coactivated T cells. The role of sCD226 on dendritic cell maturation was evaluated. The concentration of sCD226 in the sera from healthy donors (HD), pwMS, neuromyelitis optica (NMO), and Alzheimer's disease (AD) was measured.nnRESULTS: CD3/CD226-costimulation induced CD226 shedding. Addition of sCD226 to dendritic cells during their maturation led to an increased production of the pro-inflammatory cytokine interleukin (IL)-23. We observed a significant increase in sCD226 in sera from pwMS and NMO compared to HD and AD. In MS, levels were increased in both relapsing-remitting multiple sclerosis (RRMS) and secondary-progressive multiple sclerosis (SPMS) compared to clinically isolated syndrome (CIS).nnCONCLUSION: Our data suggest that T-cell activation leads to release of sCD226 that could promote inflammation and raises the possibility of using sCD226 as a biomarker for neuroinflammation.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Welsh2024,

title = {Minimal information for studies of extracellular vesicles (MISEV2023): From basic to advanced approaches},

author = {Joshua A. Welsh and Deborah C. I. Goberdhan and Lorraine O'Driscoll and Edit I. Buzas and Cherie Blenkiron and Benedetta Bussolati and Houjian Cai and Dolores Di Vizio and Tom A. P. Driedonks and Uta Erdbrügger and Juan M. Falcon‐Perez and Qing‐Ling Fu and Andrew F. Hill and Metka Lenassi and Sai Kiang Lim and Mỹ G. Mahoney and Sujata Mohanty and Andreas Möller and Rienk Nieuwland and Takahiro Ochiya and Susmita Sahoo and Ana C. Torrecilhas and Lei Zheng and Andries Zijlstra and Sarah Abuelreich and Reem Bagabas and Paolo Bergese and Esther M. Bridges and Marco Brucale and Dylan Burger and Randy P. Carney and Emanuele Cocucci and Rossella Crescitelli and Edveena Hanser and Adrian L. Harris and Norman J. Haughey and An Hendrix and Alexander R. Ivanov and Tijana Jovanovic‐Talisman and Nicole A. Kruh‐Garcia and Vroniqa Ku'ulei‐Lyn Faustino and Diego Kyburz and Cecilia Lässer and Kathleen M. Lennon and Jan Lötvall and Adam L. Maddox and Elena S. Martens‐Uzunova and Rachel R. Mizenko and Lauren A. Newman and Andrea Ridolfi and Eva Rohde and Tatu Rojalin and Andrew Rowland and Andras Saftics and Ursula S. Sandau and Julie A. Saugstad and Faezeh Shekari and Simon Swift and Dmitry Ter‐Ovanesyan and Juan P. Tosar and Zivile Useckaite and Francesco Valle and Zoltan Varga and Edwin van der Pol and Martijn J. C. van Herwijnen and Marca H. M. Wauben and Ann M. Wehman and Sarah Williams and Andrea Zendrini and Alan J. Zimmerman and and Clotilde Théry and Kenneth W. Witwer},

doi = {10.1002/jev2.12404},

issn = {2001-3078},

year  = {2024},

date = {2024-02-00},

urldate = {2024-02-00},

journal = {J of Extracellular Vesicle},

volume = {13},

number = {2},

publisher = {Wiley},

abstract = {<jats:title>Abstract</jats:title><jats:p>Extracellular vesicles (EVs), through their complex cargo, can reflect the state of their cell of origin and change the functions and phenotypes of other cells. These features indicate strong biomarker and therapeutic potential and have generated broad interest, as evidenced by the steady year‐on‐year increase in the numbers of scientific publications about EVs. Important advances have been made in EV metrology and in understanding and applying EV biology. However, hurdles remain to realising the potential of EVs in domains ranging from basic biology to clinical applications due to challenges in EV nomenclature, separation from non‐vesicular extracellular particles, characterisation and functional studies. To address the challenges and opportunities in this rapidly evolving field, the International Society for Extracellular Vesicles (ISEV) updates its ‘Minimal Information for Studies of Extracellular Vesicles’, which was first published in 2014 and then in 2018 as MISEV2014 and MISEV2018, respectively. The goal of the current document, MISEV2023, is to provide researchers with an updated snapshot of available approaches and their advantages and limitations for production, separation and characterisation of EVs from multiple sources, including cell culture, body fluids and solid tissues. In addition to presenting the latest state of the art in basic principles of EV research, this document also covers advanced techniques and approaches that are currently expanding the boundaries of the field. MISEV2023 also includes new sections on EV release and uptake and a brief discussion of in vivo approaches to study EVs. Compiling feedback from ISEV expert task forces and more than 1000 researchers, this document conveys the current state of EV research to facilitate robust scientific discoveries and move the field forward even more rapidly.</jats:p>},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{nokey,

title = {Eomes-dependent mitochondrial regulation promotes survival of pathogenic CD4+ T cells during inflammation},

author = {Emeline Joulia and Michaël F. Michieletto and Arantxa Agesta and Cindy Peillex and Virginie Girault and Anne-Louise Le Dorze and Romain Peroceschi and Florence Bucciarelli and Marion Szelechowski and Adeline Chaubet and Nawad Hakim and Rémi Marrocco and Emeline Lhuillier and Manuel Lebeurrier and Rafael J. Argüello and Abdelhadi Saoudi and Hicham El Costa and Veronique Adoue and Thierry Walzer and Jean-Emmanuel Sarry and Anne S. Dejean},

doi = {10.1084/jem.20230449},

issn = {0022-1007},

year  = {2024},

date = {2024-01-08},

journal = {Journal of Experimental Medicine},

volume = {221},

number = {2},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN27e,

title = {Intact proviruses are enriched in the colon and associated with PD-1(+)TIGIT(-) mucosal CD4(+) T cells of people with HIV-1 on antiretroviral therapy},

author = {C. Vellas and M. Nayrac and N. Collercandy and M. Requena and N. Jeanne and J. Latour and C. Dimeglio and M. Cazabat and K. Barange and L. Alric and N. Carrere and G. Martin-Blondel and J. Izopet and P. Delobel},

url = {https://www.ncbi.nlm.nih.gov/pubmed/38160480},

doi = {10.1016/j.ebiom.2023.104954},

issn = {2352-3964 (Electronic) 2352-3964 (Linking)},

year  = {2024},

date = {2024-01-01},

urldate = {2024-01-01},

journal = {EBioMedicine},

volume = {100},

pages = {104954},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN26q,

title = {Compartmentalized HIV-1 reservoir in intestinal monocytes/macrophages on antiretroviral therapy},

author = {C. Vellas and D. Martres and M. Requena and M. Nayrac and N. Collercandy and J. Latour and K. Barange and L. Alric and G. Martin-Blondel and J. Izopet and B. Lagane and P. Delobel},

url = {https://www.ncbi.nlm.nih.gov/pubmed/39561178},

doi = {10.1093/infdis/jiae557},

issn = {1537-6613 (Electronic) 0022-1899 (Linking)},

year  = {2024},

date = {2024-01-01},

urldate = {2024-01-01},

journal = {J Infect Dis},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN4510,

title = {Characterization of virus‒host recombinant variants of the hepatitis E virus},

author = {O. Paronetto and C. Allioux and C. Dimeglio and L. Lobjois and N. Jeanne and N. Ranger and J. Boineau and M. Pucelle and S. Demmou and F. Abravanel and S. Chapuy-Regaud and J. Izopet and S. Lhomme},

url = {https://www.ncbi.nlm.nih.gov/pubmed/38712945},

doi = {10.1128/jvi.00295-24},

issn = {1098-5514 (Electronic) 0022-538X (Linking)},

year  = {2024},

date = {2024-01-01},

urldate = {2024-01-01},

journal = {J Virol},

volume = {98},

number = {6},

pages = {e0029524},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Briand-Mesange2024,

title = {From Classical to Alternative Pathways of 2-Arachidonoylglycerol Synthesis: AlterAGs at the Crossroad of Endocannabinoid and Lysophospholipid Signaling},

author = {Fabienne Briand-Mésange and Isabelle Gennero and Juliette Salles and Stéphanie Trudel and Lionel Dahan and Jérôme Ausseil and Bernard Payrastre and Jean Pierre Salles and Hugues Chap},

doi = {10.3390/molecules29153694},

issn = {14203049},

year  = {2024},

date = {2024-01-01},

urldate = {2024-01-01},

journal = {Molecules},

volume = {29},

number = {15},

abstract = {2-arachidonoylglycerol (2-AG) is the most abundant endocannabinoid (EC), acting as a full agonist at both CB1 and CB2 cannabinoid receptors. It is synthesized on demand in postsynaptic membranes through the sequential action of phosphoinositide-specific phospholipase Cβ1 (PLCβ1) and diacylglycerol lipase α (DAGLα), contributing to retrograde signaling upon interaction with presynaptic CB1. However, 2-AG production might also involve various combinations of PLC and DAGL isoforms, as well as additional intracellular pathways implying other enzymes and substrates. Three other alternative pathways of 2-AG synthesis rest on the extracellular cleavage of 2-arachidonoyl-lysophospholipids by three different hydrolases: glycerophosphodiesterase 3 (GDE3), lipid phosphate phosphatases (LPPs), and two members of ecto-nucleotide pyrophosphatase/phosphodiesterases (ENPP6–7). We propose the names of AlterAG-1, -2, and -3 for three pathways sharing an ectocellular localization, allowing them to convert extracellular lysophospholipid mediators into 2-AG, thus inducing typical signaling switches between various G-protein-coupled receptors (GPCRs). This implies the critical importance of the regioisomerism of both lysophospholipid (LPLs) and 2-AG, which is the object of deep analysis within this review. The precise functional roles of AlterAGs are still poorly understood and will require gene invalidation approaches, knowing that both 2-AG and its related lysophospholipids are involved in numerous aspects of physiology and pathology, including cancer, inflammation, immune defenses, obesity, bone development, neurodegeneration, or psychiatric disorders.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN2487,

title = {Altered X-chromosome inactivation predisposes to autoimmunity},

author = {Huret, C. and Ferraye, L. and David, A. and Mohamed, M. and Valentin, N. and Charlotte, F. and Savignac, M. and Goodhardt, M. and Guery, J. C. and Rougeulle, C. and Morey, C.},

url = {https://www.ncbi.nlm.nih.gov/pubmed/38701219},

doi = {10.1126/sciadv.adn6537},

issn = {2375-2548 (Electronic) 2375-2548 (Linking)},

year  = {2024},

date = {2024-01-01},

urldate = {2024-01-01},

journal = {Sci Adv},

volume = {10},

number = {18},

pages = {eadn6537},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN2480,

title = {Sexual dimorphism in skin immunity is mediated by an androgen-ILC2-dendritic cell axis},

author = {Chi, L. and Liu, C. and Gribonika, I. and Gschwend, J. and Corral, D. and Han, S. J. and Lim, A. I. and Rivera, C. A. and Link, V. M. and Wells, A. C. and Bouladoux, N. and Collins, N. and Lima-Junior, D. S. and Enamorado, M. and Rehermann, B. and Laffont, S. and Guery, J. C. and Tussiwand, R. and Schneider, C. and Belkaid, Y.},

url = {https://www.ncbi.nlm.nih.gov/pubmed/38574174},

doi = {10.1126/science.adk6200},

issn = {1095-9203 (Electronic) 0036-8075 (Linking)},

year  = {2024},

date = {2024-01-01},

urldate = {2024-01-01},

journal = {Science},

volume = {384},

number = {6692},

pages = {eadk6200},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN2122,

title = {The Prevalence Of Osteoporosis Is Low in Adult Cutaneous Mastocytosis Patients},

author = {Y. Degboe and M. Severino-Freire and G. Couture and P. A. Apoil and N. Gaudenzio and O. Hermine and A. Ruyssen-Witrand and C. Paul and M. Laroche and A. Constantin and C. B. Livideanu},

url = {https://www.ncbi.nlm.nih.gov/pubmed/38423295},

doi = {10.1016/j.jaip.2024.02.021},

issn = {2213-2201 (Electronic)},

year  = {2024},

date = {2024-01-01},

urldate = {2024-01-01},

journal = {J Allergy Clin Immunol Pract},

volume = {12},

number = {5},

pages = {1306-1312},

abstract = {BACKGROUND: Systemic mastocytosis (SM) is a clonal disorder of mast cells (MCs) frequently associated with vertebral osteoporosis (OP) and subsequent vertebral fractures (VFs). The natural history of this OP remains unclear. Importantly, we do not know whether OP represents an early event triggered alongside MC abnormalities, and whether MC clonality is sufficient to trigger osteoporosis. OBJECTIVE: To describe OP in patients with medullar clonality in cutaneous mastocytosis (CM) and monoclonal mast cell activation syndrome (MMAS) and to compare their osteoporosis characteristics with those of nonadvanced SM patients (bone marrow mastocytosis and indolent systemic mastocytosis). METHODS: We retrospectively analyzed clinical, biological, and densitometric data of 27 CM, 13 MMAS, and 135 SM patients from the Mastocytosis Expert Center (CEREMAST) in Toulouse, France. RESULTS: The OP (respectively 3.7, 30.8, and 34.1%) and VFs (0.0%, 15.4%, and 20%) were less frequent in CM than in MMAS and SM, despite the presence of clonal MCs in the bone marrow. Most patients with OP and VFs in the non-SM groups had the usual risk factors for OP. Interestingly, the only non-SM patient with a typical SM-like OP had high bone marrow tryptase, developed bone marrow KIT mutation during follow-up, and had a family history of SM. Our data show that OP is not a common clinical finding in CM but is frequent in MMAS. When OP and VFs occur in CM and MMAS patients, they differ from the usual phenotype of SM bone fragility. CONCLUSIONS: Our findings suggest that, in most CM patients, the meaning and management of OP differs from that of OP in MMAS and nonadvanced SM. Prospective longitudinal studies and the validation of predictors are needed to identify CM and MMAS patients developing SM-related OP.},

note = {Degboe, Yannick 

Severino-Freire, Maella 

Couture, Guillaume 

Apoil, Pol-Andre 

Gaudenzio, Nicolas 

Hermine, Olivier 

Ruyssen-Witrand, Adeline 

Paul, Carle 

Laroche, Michel 

Constantin, Arnaud 

Livideanu, Cristina Bulai 

eng 

Research Support, Non-U.S. Gov't 

2024/03/01 

J Allergy Clin Immunol Pract. 2024 May;12(5):1306-1312. doi: 10.1016/j.jaip.2024.02.021. Epub 2024 Feb 27.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN2123,

title = {Diagnosis and treatment of Tropheryma whipplei infection in patients with inflammatory rheumatic disease: Data from the French Tw-IRD registry},

author = {D. Caillet Portillo and X. Puechal and M. Masson and M. Kostine and A. Michaut and A. Ramon and D. Wendling and N. Costedoat-Chalumeau and P. Richette and H. Marotte and J. Vix-Portet and J. J. Dubost and S. Ottaviani and G. Mouterde and A. Grasland and A. Frazier and V. Germain and F. Coury and A. Tournadre and M. Soubrier and L. Cavalie and P. Brevet and L. Zabraniecki and B. Jamard and G. Couture and L. Arnaud and C. Richez and Y. Degboe and A. Ruyssen-Witrand and A. Constantin},

url = {https://www.ncbi.nlm.nih.gov/pubmed/38141787},

doi = {10.1016/j.jinf.2023.12.010},

issn = {1532-2742 (Electronic) 0163-4453 (Linking)},

year  = {2024},

date = {2024-01-01},

urldate = {2024-01-01},

journal = {J Infect},

volume = {88},

number = {2},

pages = {132-138},

abstract = {OBJECTIVES: Tropheryma whipplei infection can manifest as inflammatory joint symptoms, which can lead to misdiagnosis of inflammatory rheumatic disease and the use of disease-modifying antirheumatic drugs. We investigated the impact of diagnosis and treatment of Tropheryma whipplei infection in patients with inflammatory rheumatic disease. METHODS: We initiated a registry including patients with disease-modifying antirheumatic drugs-treated inflammatory rheumatic disease who were subsequently diagnosed with Tropheryma whipplei infection. We collected clinical, biological, treatment data of the inflammatory rheumatic disease, of Tropheryma whipplei infection, and impact of antibiotics on the evolution of inflammatory rheumatic disease. RESULTS: Among 73 inflammatory rheumatic disease patients, disease-modifying antirheumatic drugs initiation triggered extra-articular manifestations in 27% and resulted in stabilisation (51%), worsening (34%), or improvement (15%) of inflammatory rheumatic disease. At the diagnosis of Tropheryma whipplei infection, all patients had rheumatological symptoms (mean age 58 years, median inflammatory rheumatic disease duration 79 months), 84% had extra-rheumatological manifestations, 93% had elevated C-reactive protein, and 86% had hypoalbuminemia. Treatment of Tropheryma whipplei infection consisted mainly of doxycycline plus hydroxychloroquine, leading to remission of Tropheryma whipplei infection in 79% of cases. Antibiotic treatment of Tropheryma whipplei infection was associated with remission of inflammatory rheumatic disease in 93% of cases and enabled disease-modifying antirheumatic drugs and glucocorticoid discontinuation in most cases. CONCLUSIONS: Tropheryma whipplei infection should be considered in inflammatory rheumatic disease patients with extra-articular manifestations, elevated C-reactive protein, and/or hypoalbuminemia before disease-modifying antirheumatic drugs initiation or in inflammatory rheumatic disease patients with an inadequate response to one or more disease-modifying antirheumatic drugs. Positive results of screening and diagnostic tests for Tropheryma whipplei infection involve antibiotic treatment, which is associated with complete recovery of Tropheryma whipplei infection and rapid remission of inflammatory rheumatic disease, allowing disease-modifying antirheumatic drugs and glucocorticoid discontinuation.},

note = {Caillet Portillo, Damien 

Puechal, Xavier 

Masson, Maeva 

Kostine, Marie 

Michaut, Alexia 

Ramon, Andre 

Wendling, Daniel 

Costedoat-Chalumeau, Nathalie 

Richette, Pascal 

Marotte, Hubert 

Vix-Portet, Justine 

Dubost, Jean-Jacques 

Ottaviani, Sebastien 

Mouterde, Gael 

Grasland, Anne 

Frazier, Aline 

Germain, Vincent 

Coury, Fabienne 

Tournadre, Anne 

Soubrier, Martin 

Cavalie, Laurent 

Brevet, Pauline 

Zabraniecki, Laurent 

Jamard, Benedicte 

Couture, Guillaume 

Arnaud, Laurent 

Richez, Christophe 

Degboe, Yannick 

Ruyssen-Witrand, Adeline 

Constantin, Arnaud 

eng 

England 

2023/12/24 

J Infect. 2024 Feb;88(2):132-138. doi: 10.1016/j.jinf.2023.12.010. Epub 2023 Dec 22.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Salles2024,

title = {Differential DNA methylation in iPSC-derived dopaminergic neurons: a step forward on the role of SNORD116 microdeletion in the pathophysiology of addictive behavior in Prader-Willi syndrome},

author = {Juliette Salles and Sanaa Eddiry and Saber Amri and Mélissa Galindo and Emmanuelle Lacassagne and Simon George and Xavier Mialhe and Émeline Lhuillier and Nicolas Franchitto and Freddy Jeanneteau and Isabelle Gennero and Jean Pierre Salles and Maithé Tauber},

doi = {10.1038/s41380-024-02542-4},

issn = {14765578},

year  = {2024},

date = {2024-01-01},

urldate = {2024-01-01},

journal = {Molecular Psychiatry},

number = {March},

publisher = {Springer US},

abstract = {Introduction: A microdeletion including the SNORD116 gene (SNORD116 MD) has been shown to drive the Prader-Willi syndrome (PWS) features. PWS is a neurodevelopmental disorder clinically characterized by endocrine impairment, intellectual disability and psychiatric symptoms such as a lack of emotional regulation, impulsivity, and intense temper tantrums with outbursts. In addition, this syndrome is associated with a nutritional trajectory characterized by addiction-like behavior around food in adulthood. PWS is related to the genetic loss of expression of a minimal region that plays a potential role in epigenetic regulation. Nevertheless, the role of the SNORD116 MD in DNA methylation, as well as the impact of the oxytocin (OXT) on it, have never been investigated in human neurons. Methods: We studied the methylation marks in induced pluripotent stem-derived dopaminergic neurons carrying a SNORD116 MD in comparison with those from an age-matched adult healthy control. We also performed identical neuron differentiation in the presence of OXT. We performed a genome-wide DNA methylation analysis from the iPSC-derived dopaminergic neurons by reduced-representation bisulfite sequencing. In addition, we performed RNA sequencing analysis in these iPSC-derived dopaminergic neurons differentiated with or without OXT. Results: The analysis revealed that 153,826 cytosines were differentially methylated between SNORD116 MD neurons and control neurons. Among the differentially methylated genes, we determined a list of genes also differentially expressed. Enrichment analysis of this list encompassed the dopaminergic system with COMT and SLC6A3. COMT displayed hypermethylation and under-expression in SNORD116 MD, and SLC6A3 displayed hypomethylation and over-expression in SNORD116 MD. RT-qPCR confirmed significant over-expression of SLC6A3 in SNORD116 MD neurons. Moreover, the expression of this gene was significantly decreased in the case of OXT adjunction during the differentiation. Conclusion: SNORD116 MD dopaminergic neurons displayed differential methylation and expression in the COMT and SLC6A3 genes, which are related to dopaminergic clearance.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{lacouture_lfa-1_2024,

title = {LFA-1 nanoclusters integrate TCR stimulation strength to tune T-cell cytotoxic activity},

author = {Claire Lacouture and Beatriz Chaves and Delphine Guipouy and Raïssa Houmadi and Valérie Duplan-Eche and Sophie Allart and Nicolas Destainville and Loïc Dupré},

url = {https://www.nature.com/articles/s41467-024-44688-3},

doi = {10.1038/s41467-024-44688-3},

issn = {2041-1723},

year  = {2024},

date = {2024-01-01},

urldate = {2024-01-01},

journal = {Nature Communications},

volume = {15},

number = {1},

pages = {407},

abstract = {T-cell cytotoxic function relies on the cooperation between the highly specific but poorly adhesive T-cell receptor (TCR) and the integrin LFA-1. How LFA-1-mediated adhesion may scale with TCR stimulation strength is ill-defined. Here, we show that LFA-1 conformation activation scales with TCR stimulation to calibrate human T-cell cytotoxicity. Super-resolution microscopy analysis reveals that >1000 LFA-1 nanoclusters provide a discretized platform at the immunological synapse to translate TCR engagement and density of the LFA-1 ligand ICAM-1 into graded adhesion. Indeed, the number of high-affinity conformation LFA-1 nanoclusters increases as a function of TCR triggering strength. Blockade of LFA-1 conformational activation impairs adhesion to target cells and killing. However, it occurs at a lower TCR stimulation threshold than lytic granule exocytosis implying that it licenses, rather than directly controls, the killing decision. We conclude that the organization of LFA-1 into nanoclusters provides a calibrated system to adjust T-cell killing to the antigen stimulation strength.},

note = {Number: 1 

Publisher: Nature Publishing Group},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Malnou2023,

title = {Editorial: Recent highlights in the development of therapeutic antiviral strategies},

author = {Cécile E. Malnou and Gaëtan Ligat},

doi = {10.3389/fmicb.2023.1338999},

issn = {1664-302X},

year  = {2023},

date = {2023-12-05},

urldate = {2023-12-05},

journal = {Front. Microbiol.},

volume = {14},

publisher = {Frontiers Media SA},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Scholaert2023,

title = {Pre-print | Multi-modal profiling of biostabilized human skin modules reveals a coordinated ecosystem response to injected mRNA-1273 COVID-19 vaccine},

author = {Manon Scholaert and Mathias Peries and Emilie Braun and Jeremy Martin and Nadine Serhan and Alexia Loste and Audrey Bruner and Lilian Basso and Benoit Chaput and Eric Merle and Pascal Descargues and Emeline Pages and Nicolas Gaudenzio},

url = {https://www.biorxiv.org/content/10.1101/2023.09.22.558940v1},

year  = {2023},

date = {2023-09-27},

journal = {bioRxiv},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid37748654,

title = {Widespread monoclonal IgE antibody convergence to an immunodominant, proanaphylactic Ara h 2 epitope in peanut allergy},

author = {Derek Croote and Joyce J W Wong and Cyprien Pecalvel and Edouard Leveque and Natacha Casanovas and Jasper B J Kamphuis and Paige Creeks and Johanna Romero and Saba Sohail and Daniel Bedinger and Kari C Nadeau and Rebecca S Chinthrajah and Laurent L Reber and Henry B Lowman},

doi = {10.1016/j.jaci.2023.08.035},

issn = {1097-6825},

year  = {2023},

date = {2023-09-01},

urldate = {2023-09-01},

journal = {J Allergy Clin Immunol},

abstract = {BACKGROUND: Despite their central role in peanut allergy, human monoclonal IgE antibodies have eluded characterization.nnOBJECTIVE: We sought to define the sequences, affinities, clonality, and functional properties of human monoclonal IgE antibodies in peanut allergy.nnMETHODS: We applied our single-cell RNA sequencing-based SEQ SIFTER discovery platform to samples from allergic individuals who varied by age, sex, ethnicity, and geographic location in order to understand commonalities in the human IgE response to peanut allergens. Select antibodies were then recombinantly expressed and characterized for their allergen and epitope specificity, affinity, and functional properties.nnRESULTS: We found striking convergent evolution of IgE monoclonal antibodies (mAbs) from several clonal families comprising both memory B cells and plasmablasts. These antibodies bound with subnanomolar affinity to the immunodominant peanut allergen Ara h 2, specifically a linear, repetitive motif. Further characterization of these mAbs revealed their ability to single-handedly cause affinity-dependent degranulation of human mast cells and systemic anaphylaxis on peanut allergen challenge in humanized mice. Finally, we demonstrated that these mAbs, reengineered as IgGs, inhibit significant, but variable, amounts of Ara h 2- and peanut-mediated degranulation of mast cells sensitized with allergic plasma.nnCONCLUSIONS: Convergent evolution of IgE mAbs in peanut allergy is a common phenomenon that can reveal immunodominant epitopes on major allergenic proteins. Understanding the functional properties of these molecules is key to developing therapeutics, such as competitive IgG inhibitors, that are able to stoichiometrically outcompete endogenous IgE for allergen and thereby prevent allergic cascade in cases of accidental allergen exposure.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}