@article{lacouture_kinetic_2023,

title = {Kinetic measurements of human CD8+ Ŧ cell cytotoxic activity in a 384-well plate format},

author = {Lacouture, Claire and Prunier, Guilhèn and Dupré, Loïc},

doi = {10.1016/bs.mcb.2022.07.014},

issn = {0091-679X},

year  = {2023},

date = {2023-01-01},

journal = {Methods Cell Biol},

volume = {178},

pages = {121--133},

abstract = {The elimination of infected or cancerous cells by CD8+ cytotoxic T lymphocytes (CTL) is a crucial effector mechanism of the immune system. Upon antigen recognition, CTL stop migrating, establish a tight contact with target cells and deliver cytotoxic molecules such as perforin and granzymes that lead to target cell apoptosis. The ability of CTL to control a population of infected cells or a tumor depends on multiple parameters, such as the relative numbers of CTL and target cells, the intrinsic cytotoxic activity of CTL, the intrinsic resistance of target cells and the repertoire of immune checkpoints tuning cytotoxic activity at the CTL:target cell interface. In this context, in vitro assays to precisely measure CTL:target cell interactions and cytotoxic activity over time are required to monitor natural or therapeutic responses. We here present an image-based method that allows recording of positions and survival of CTL and target cells over time in a high-throughput format. The protocol relies on the staining of CTL and target cells with fluorescent dyes and the automated imaging of cells deposited in wells of a 384-well plate with an automated cell imaging device. We discuss potential applications offered by the kinetic assessment of CTL cytotoxic activity in a high-throughput format.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{prunier_metrics_2023,

title = {Metrics of 2D immunological synapses in human Ŧ cells via high-content confocal cell imaging},

author = {Prunier, Guilhèn and Chaves, Beatriz and Lacouture, Claire and Dupré, Loïc},

doi = {10.1016/bs.mcb.2022.07.013},

issn = {0091-679X},

year  = {2023},

date = {2023-01-01},

journal = {Methods Cell Biol},

volume = {178},

pages = {107--120},

abstract = {Immunological synapses (IS) are the privileged site of complex information transfer between T cells and antigen presenting cells. IS are highly structured in terms of actin and tubulin cytoskeleton organization, receptor and proximal signal patterning, and intracellular organelle polarization. The magnitude and quality of T cell responses upon antigen recognition is dependent on IS molecular organization. For that reason, methods to precisely assess IS parameters are crucial to monitor T cell activation and function in health and disease, but also for T cell centered therapeutic intervention. Confocal and super-resolution microscopy approaches have allowed to characterize the complex structure of the T cell IS. However, those approaches suffer from a low-throughput and low-content format precluding multi-parametric classification of IS across large numbers of samples or stimulatory conditions. Here, we present a protocol of high-content confocal cell imaging in a 384-well plate format adapted to the unbiased analysis of primary T cells forming IS over pre-coated stimulatory molecules. The protocol focuses on the staining of F-actin, pericentrin and granzyme B in CD8+ T cells, but is transposable to other IS molecular markers and lymphocyte subsets. We discuss potential applications offered by the multi-parametric characterization of T cell IS in a high-throughput format.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{c,

title = {Evolution and spread of Plasmodium falciparum mutations associated with resistance to sulfadoxine-pyrimethamine in central Africa: a cross-sectional study},

author = {Guemas, E. and Coppee, R. and Menard, S. and du Manoir, M. and Nsango, S. and Makaba Mvumbi, D. and Nakoune, E. and Eboumbou Moukoko, C. E. and Bouyou Akotet, M. K. and Mirabeau, T. Y. and Manguin, S. and Malekita Yobi, D. and Akiana, J. and Kouna, L. C. and Mawili Mboumba, D. P. and Voumbo-Matoumona, D. F. and Otam, A. L. and Rubbo, P. A. and Lombart, J. P. and Kwanai, E. and Cohen, O. and Iriart, X. and Ayong, L. and Lekana-Douki, J. B. and Ariey, F. and Berry, A.},

year  = {2023},

date = {2023-01-01},

journal = {Lancet Microbe},

abstract = {BACKGROUND: Efficacy of sulfadoxine-pyrimethamine, the malaria chemoprophylaxis used in pregnant women, and in children when combined with amodiaquine, is threatened by the accumulation of mutations in the Plasmodium falciparum dihydropteroate synthase (pfdhps) and dihydrofolate reductase (pfdhfr) genes. Data on the prevalence of resistant alleles in central Africa and the new pfdhps I431V mutation, particularly associated with other mutations to form the pfdhps vagKgs allele, are scarce. We explored the frequency and geographical distribution of pfdhps and pfdhfr mutations in central Africa in 2014-18, and assessed the evolutionary origin of the vagKgs allele. METHODS: Samples were collected at 18 health-care centres in seven countries (Angola, Cameroon, Central African Republic, Democratic Republic of the Congo, Gabon, Nigeria, and Republic of the Congo) from patients who showed possible symptoms of malaria between March 1, 2014, and Oct 31, 2018. Samples that were positive for P falciparum were transported to a laboratory in Toulouse, France, and genotyped. The frequency of pfdhfr and pfdhps mutations was studied in 1749 samples. Microsatellites in pfdhps flanking regions and whole-genome analysis compared with parasite genomes from the data-sharing network MalariaGEN were performed on samples carrying the vagKgs allele. FINDINGS: Mapping of the prevalence of single nucleotide polymorphisms and corresponding alleles of pfdhfr and pfdhps showed a substantial spread of alleles associated with sulfadoxine-pyrimethamine resistance in central Africa during the 2014-18 period, especially an increase going west to east in pfdhps alleles carrying the K540E and A581G mutations. A high prevalence of the pfdhps I431V mutation was observed in Cameroon (exceeding 50% in the northern region) and Nigeria. Genomic analysis showed a recent African emergence and a clonal expansion of the most frequent pfdhps vagKgs allele. INTERPRETATION: Reduced sulfadoxine-pyrimethamine efficacy due to increased resistance is a worrying situation, especially because the malaria transmission level is high in central Africa. Although the resistance phenotype remains to be confirmed, the emergence and spread of the vagKgs allele in west and central Africa could challenge the use of sulfadoxine-pyrimethamine. FUNDING: Toulouse Institute for Infectious and Inflammatory Diseases.},

note = {doi: 10.1016/S2666-5247(23)00211-2.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{c,

title = {Effect of sulfadoxine-pyrimethamine chemoprophylaxis in pregnant women on selection of the new P. falciparum dhps quintuple mutant carrying the I431V mutation},

author = {Cohen, O. and Guemas, E. and Menard, S. and Tsague Kenfack, M. and Talom Ngassa, C. and Iriart, X. and Bidzogo Lebobo, M. and Ondobo Ekae, C. and Eboumbou, C. and Tiyou Kenmeni, C. and Berry, A.},

year  = {2023},

date = {2023-01-01},

journal = {J Antimicrob Chemother},

volume = {78},

number = {3},

pages = {665-668},

abstract = {BACKGROUND: A new mutation in the Plasmodium falciparum dihydropteroate synthetase gene (pfdhps), I431V, has been identified in several countries of Central and West Africa. This mutation is mostly found in association with four other SNPs on pfdhps (S436A, A437G, A581G and A613S), forming a quintuple mutant (vagKgs) and almost always associated with the Plasmodium falciparum dihydrofolate reductase gene (pfdhfr) CirnI (C50R, N51I, S108N) triple mutant. To date, nothing is known about the impact of this new pfdhps genotype on sulfadoxine-pyrimethamine (SP) resistance. OBJECTIVES: We sought to assess the prevalence of this pfdhps vagKgs quintuple mutant in two groups of pregnant women with malaria, one that took intermittent preventive treatment with sulfadoxine-pyrimethamine (IPTp-SP) and one that did not. METHODS: The pfdhfr and pfdhps genes from Plasmodium falciparum isolates collected in Yaounde (Cameroon) from pregnant women with symptomatic malaria under IPTp-SP or not, were sequenced. RESULTS: Of 159 patients evaluated, 70 had already taken SP during pregnancy and 89 had never taken SP. Only the vagKgs allele was significantly overrepresented in the SP+ group (21.4% versus 3.4%; P < 0.001), whereas the ISgKAA mutant, widely distributed in this area and known to be less susceptible to SP, tended to be less abundant in this group (48.6% versus 64.0%; P = 0.0503). CONCLUSIONS: We found a strong overrepresentation of the CirnI/vagKgs haplotype in the IPTp-SP pregnant group, suggesting a high level of resistance of this mutant to SP. This could compromise not only the effectiveness of IPTp-SP but also the seasonal malaria chemoprevention of young children, now widely implemented.},

note = { doi: 10.1093/jac/dkac432.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN4495,

title = {The pressing need for a global HEV vaccine},

author = {Peron, J. M. and Larrue, H. and Izopet, J. and Buti, M.},

url = {https://www.ncbi.nlm.nih.gov/pubmed/37003442},

doi = {10.1016/j.jhep.2023.03.024},

issn = {1600-0641 (Electronic) 

0168-8278 (Linking)},

year  = {2023},

date = {2023-01-01},

journal = {J Hepatol},

volume = {79},

number = {3},

pages = {876-880},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN2418,

title = {TLR8 escapes X chromosome inactivation in human monocytes and CD4(+) T cells},

author = {Youness, A. and Cenac, C. and Faz-Lopez, B. and Grunenwald, S. and Barrat, F. J. and Chaumeil, J. and Mejia, J. E. and Guery, J. C.},

url = {https://www.ncbi.nlm.nih.gov/pubmed/37723501},

doi = {10.1186/s13293-023-00544-5},

issn = {2042-6410 (Electronic) 

2042-6410 (Linking)},

year  = {2023},

date = {2023-01-01},

journal = {Biol Sex Differ},

volume = {14},

number = {1},

pages = {60},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN2417,

title = {Immunological and translational key challenges in systemic lupus erythematosus: A symposium update},

author = {Renaudineau, Y. and Muller, S. and Hedrich, C. M. and Chauveau, D. and Belliere, J. and De Almeida, S. and Damoiseaux, J. and Scherlinger, M. and Guery, J. C. and Sailler, L. and Bost, C.},

url = {https://www.ncbi.nlm.nih.gov/pubmed/37065621},

doi = {10.1016/j.jtauto.2023.100199},

issn = {2589-9090 (Electronic) 

2589-9090 (Linking)},

year  = {2023},

date = {2023-01-01},

journal = {J Transl Autoimmun},

volume = {6},

pages = {100199},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN2416,

title = {Influence of X chromosome in sex-biased autoimmune diseases},

author = {Miquel, C. H. and Faz-Lopez, B. and Guery, J. C.},

url = {https://www.ncbi.nlm.nih.gov/pubmed/36641351},

doi = {10.1016/j.jaut.2023.102992},

issn = {1095-9157 (Electronic) 

0896-8411 (Linking)},

year  = {2023},

date = {2023-01-01},

journal = {J Autoimmun},

volume = {137},

pages = {102992},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN2415,

title = {B cell-intrinsic TLR7 signaling is required for neutralizing antibody responses to SARS-CoV-2 and pathogen-like COVID-19 vaccines},

author = {Miquel, C. H. and Abbas, F. and Cenac, C. and Foret-Lucas, C. and Guo, C. and Ducatez, M. and Joly, E. and Hou, B. and Guery, J. C.},

url = {https://www.ncbi.nlm.nih.gov/pubmed/37438976},

doi = {10.1002/eji.202350437},

issn = {1521-4141 (Electronic) 

0014-2980 (Linking)},

year  = {2023},

date = {2023-01-01},

journal = {Eur J Immunol},

pages = {e2350437},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN2414,

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  = {2023},

date = {2023-01-01},

journal = {Allergy},

volume = {78},

number = {3},

pages = {879-882},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN2413,

title = {The Influence of Sex Hormones and X Chromosome in Immune Responses},

author = {Anesi, N. and Miquel, C. H. and Laffont, S. and Guery, J. C.},

url = {https://www.ncbi.nlm.nih.gov/pubmed/37695424},

doi = {10.1007/978-3-031-35139-6_2},

issn = {0070-217X (Print) 

0070-217X (Linking)},

year  = {2023},

date = {2023-01-01},

journal = {Curr Top Microbiol Immunol},

volume = {441},

pages = {21-59},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{c,

title = {The apicoplast is important for the viability and persistence of Toxoplasma gondii bradyzoites},

author = {Sanchez, S. G. and Bassot, E. and Cerutti, A. and Mai Nguyen, H. and Aida, A. and Blanchard, N. and Besteiro, S.},

year  = {2023},

date = {2023-01-01},

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

volume = {120},

number = {34},

pages = {e2309043120},

abstract = {Toxoplasma gondii is responsible for toxoplasmosis, a disease that can be serious when contracted during pregnancy, but can also be a threat for immunocompromised individuals. Acute infection is associated with the tachyzoite form that spreads rapidly within the host. However, under stress conditions, some parasites can differentiate into cyst-forming bradyzoites, residing mainly in the central nervous system, retina and muscle. Because this latent form of the parasite is resistant to all currently available treatments, and is central to persistence and transmission of the parasite, specific therapeutic strategies targeting this developmental stage need to be found. T. gondii contains a plastid of endosymbiotic origin called the apicoplast, which is an appealing drug target because it is essential for tachyzoite viability and contains several key metabolic pathways that are largely absent from the mammalian host. Its function in bradyzoites, however, is unknown. Our objective was thus to study the contribution of the apicoplast to the viability and persistence of bradyzoites during chronic toxoplasmosis. We have used complementary strategies based on stage-specific promoters to generate conditional bradyzoite mutants of essential apicoplast genes. Our results show that specifically targeting the apicoplast in both in vitro or in vivo-differentiated bradyzoites leads to a loss of long-term bradyzoite viability, highlighting the importance of this organelle for this developmental stage. This validates the apicoplast as a potential area to look for therapeutic targets in bradyzoites, with the aim to interfere with this currently incurable parasite stage.},

note = {doi:10.1073/pnas.2309043120},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{dupre_deciphering_2023,

title = {Deciphering actin remodelling in immune cells through the prism of actin-related inborn errors of immunity},

author = {Dupré, Loïc and Prunier, Guilhèn},

doi = {10.1016/j.ejcb.2022.151283},

issn = {1618-1298},

year  = {2023},

date = {2023-01-01},

journal = {Eur J Cell Biol},

volume = {102},

number = {1},

pages = {151283},

abstract = {Actin cytoskeleton remodelling drives cell motility, cell to cell contacts, as well as membrane and organelle dynamics. Those cellular activities operate at a particularly high pace in immune cells since these cells migrate through various tissues, interact with multiple cellular partners, ingest microorganisms and secrete effector molecules. The central and multifaceted role of actin cytoskeleton remodelling in sustaining immune cell tasks in humans is highlighted by rare inborn errors of immunity due to mutations in genes encoding proximal and distal actin regulators. In line with the specificity of some of the actin-based processes at work in immune cells, the expression of some of the affected genes, such as WAS, ARPC1B and HEM1 is restricted to the hematopoietic compartment. Exploration of these natural deficiencies highlights the fact that the molecular control of actin remodelling is tuned distinctly in the various subsets of myeloid and lymphoid immune cells and sustains different networks associated with a vast array of specialized tasks. Furthermore, defects in individual actin remodelling proteins are usually associated with partial cellular impairments highlighting the plasticity of actin cytoskeleton remodelling. This review covers the roles of disease-associated actin regulators in promoting the actin-based processes of immune cells. It focuses on the specific molecular function of those regulators across various immune cell subsets and in response to different stimuli. Given the fact that numerous immune-related actin defects have only been characterized recently, we further discuss the challenges lying ahead to decipher the underlying patho-mechanisms.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{kostel_bal_biallelic_2023,

title = {Biallelic NFATC1 mutations cause an inborn error of immunity with impaired CD8+ Ŧ-cell function and perturbed glycolysis},

author = {Kostel Bal, Sevgi and Giuliani, Sarah and Block, Jana and Repiscak, Peter and Hafemeister, Christoph and Shahin, Tala and Kasap, Nurhan and Ransmayr, Bernhard and Miao, Yirun and van de Wetering, Cheryl and Frohne, Alexandra and Jimenez-Heredia, Raul and Schuster, Michael K. and Zoghi, Samaneh and Hertlein, Vanessa and Thian, Marini and Bykov, Aleksandr and Babayeva, Royala and Bilgic Eltan, Sevgi and Karakoc-Aydiner, Elif and Shaw, Lisa E. and Chowdhury, Iftekhar and Varjosalo, Markku and Argüello, Rafael Jose and Farlik, Matthias and Ozen, Ahmet and Serfling, Edgar Albert Ernst and Dupré, Loïc and Bock, Christoph and Halbritter, Florian and Hannich, J. Thomas and Castanon, Irinka and Kraakman, Michael J. and Baris, Safa and Boztug, Kaan},

doi = {10.1182/blood.2022018303},

issn = {1528-0020},

year  = {2023},

date = {2023-01-01},

journal = {Blood},

pages = {blood.2022018303},

abstract = {The NFAT family of transcription factors plays central roles in adaptive immunity in murine models, however, their contribution to human immune homeostasis remains poorly defined. In a multigenerational pedigree, we identified three patients carrying germline biallelic missense variants in NFATC1, presenting with recurrent infections, hypogammaglobulinemia and decreased antibody responses. The compound heterozygous NFATC1 variants identified in the patients caused decreased stability and reduced binding of DNA and interacting proteins. We observed defects in early activation and proliferation of T and B cells from these patients, amenable to reconstitution upon genetic rescue. Following stimulation, T-cell activation and proliferation were impaired, reaching that of healthy controls with delay indicative of an adaptive capacity of the cells. Assessment of the metabolic capacity of patient T cells, revealed that NFATc1-dysfunction rendered T cells unable to engage in glycolysis following stimulation, although oxidative metabolic processes were intact. We hypothesized that NFATc1-mutant T cells could compensate for the energy deficit due to defective glycolysis by enhanced lipid metabolism as an adaptation, leading to a delayed, but not lost activation responses. Indeed, we observed increased 13C-labelled palmitate incorporation into citrate indicating higher fatty acid oxidation and we demonstrated that metformin and rosiglitazone improved patient T-cell effector functions. Collectively, enabled by our molecular dissection of NFATC1 mutations and extending the role of NFATc1 in human immunity beyond receptor signaling, and reveal evidence of metabolic plasticity in the context of impaired glycolysis observed in patient T cells to remedy delayed effector responses.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Martin2022,

title = {Placental extracellular vesicles in maternal-fetal communication during pregnancy},

author = {Charlène Martin and Mathilde Bergamelli and Cécile E. Malnou and Gisela D'Angelo},

doi = {10.1042/bst20220734},

issn = {1470-8752},

year  = {2022},

date = {2022-12-16},

urldate = {2022-12-16},

journal = {Biochem Soc Trans},

volume = {50},

number = {6},

pages = {1785--1795},

publisher = {Portland Press Ltd.},

abstract = {<jats:p>For several years, a growing number of studies have highlighted the pivotal role of placental extracellular vesicles (EVs) throughout pregnancy. These membrane nanovesicles, heterogeneous in nature, composition and origin, are secreted by several trophoblastic cell types and are found in both the maternal and fetal compartments. They can be uptaken by recipient cells and drive a wide variety of physiological and pathological processes. In this review, we provide an overview of the different described roles of placental EVs in various aspects of normal pregnancy, from placenta establishment to maternal immune tolerance towards the fetus and protection against viral infections. In the second part, we present selected examples of pathological pregnancies in which placental EVs are involved, such as gestational diabetes mellitus, pre-eclampsia, and congenital infections. Since the abundance and/or composition of placental EVs is deregulated in maternal serum during pathological pregnancies, this makes them interesting candidates as non-invasive biomarkers for gestational diseases and opens a wide field of translational perspectives.</jats:p>},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Matheson2022,

title = {Multiomics analysis couples mRNA turnover and translational control of glutamine metabolism to the differentiation of the activated CD4+ T cell},

author = {Matheson, Louise S. 

and Petkau, Georg 

and S{'a}enz-Narciso, Beatriz 

and D'Angeli, Vanessa 

and McHugh, Jessica 

and Newman, Rebecca 

and Munford, Haydn 

and West, James 

and Chakraborty, Krishnendu 

and Roberts, Jennie 

and {Ł}ukasiak, Sebastian 

and D{'i}az-Mu{ñ}oz, Manuel D. 

and Bell, Sarah E. 

and Dimeloe, Sarah 

and Turner, Martin},

url = {https://doi.org/10.1038/s41598-022-24132-6},

doi = {10.1038/s41598-022-24132-6},

issn = {2045-2322},

year  = {2022},

date = {2022-11-16},

journal = {Scientific Reports},

volume = {12},

number = {1},

pages = {19657},

abstract = {The ZFP36 family of RNA-binding proteins acts post-transcriptionally to repress translation and promote RNA decay. Studies of genes and pathways regulated by the ZFP36 family in CD4+ T cells have focussed largely on cytokines, but their impact on metabolic reprogramming and differentiation is unclear. Using CD4+ T cells lacking Zfp36 and Zfp36l1, we combined the quantification of mRNA transcription, stability, abundance and translation with crosslinking immunoprecipitation and metabolic profiling to determine how they regulate T cell metabolism and differentiation. Our results suggest that ZFP36 and ZFP36L1 act directly to limit the expression of genes driving anabolic processes by two distinct routes: by targeting transcription factors and by targeting transcripts encoding rate-limiting enzymes. These enzymes span numerous metabolic pathways including glycolysis, one-carbon metabolism and glutaminolysis. Direct binding and repression of transcripts encoding glutamine transporter SLC38A2 correlated with increased cellular glutamine content in ZFP36/ZFP36L1-deficient T cells. Increased conversion of glutamine to $alpha$-ketoglutarate in these cells was consistent with direct binding of ZFP36/ZFP36L1 to Gls (encoding glutaminase) and Glud1 (encoding glutamate dehydrogenase). We propose that ZFP36 and ZFP36L1 as well as glutamine and $alpha$-ketoglutarate are limiting factors for the acquisition of the cytotoxic CD4+ T cell fate. Our data implicate ZFP36 and ZFP36L1 in limiting glutamine anaplerosis and differentiation of activated CD4+ T cells, likely mediated by direct binding to transcripts of critical genes that drive these processes.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid36048016,

title = {Broader Epstein-Barr virus-specific T cell receptor repertoire in patients with multiple sclerosis},

author = {Tilman Schneider-Hohendorf and Lisa Ann Gerdes and Béatrice Pignolet and Rachel Gittelman and Patrick Ostkamp and Florian Rubelt and Catarina Raposo and Björn Tackenberg and Marianne Riepenhausen and Claudia Janoschka and Christian Wünsch and Florence Bucciarelli and Andrea Flierl-Hecht and Eduardo Beltrán and Tania Kümpfel and Katja Anslinger and Catharina C Gross and Heidi Chapman and Ian Kaplan and David Brassat and Hartmut Wekerle and Martin Kerschensteiner and Luisa Klotz and Jan D Lünemann and Reinhard Hohlfeld and Roland Liblau and Heinz Wiendl and Nicholas Schwab},

doi = {10.1084/jem.20220650},

issn = {1540-9538},

year  = {2022},

date = {2022-11-01},

urldate = {2022-11-01},

journal = {J Exp Med},

volume = {219},

number = {11},

abstract = {Epstein-Barr virus (EBV) infection precedes multiple sclerosis (MS) pathology and cross-reactive antibodies might link EBV infection to CNS autoimmunity. As an altered anti-EBV T cell reaction was suggested in MS, we queried peripheral blood T cell receptor β chain (TCRβ) repertoires of 1,395 MS patients, 887 controls, and 35 monozygotic, MS-discordant twin pairs for multimer-confirmed, viral antigen-specific TCRβ sequences. We detected more MHC-I-restricted EBV-specific TCRβ sequences in MS patients. Differences in genetics or upbringing could be excluded by validation in monozygotic twin pairs discordant for MS. Anti-VLA-4 treatment amplified this observation, while interferon β- or anti-CD20 treatment did not modulate EBV-specific T cell occurrence. In healthy individuals, EBV-specific CD8+ T cells were of an effector-memory phenotype in peripheral blood and cerebrospinal fluid. In MS patients, cerebrospinal fluid also contained EBV-specific central-memory CD8+ T cells, suggesting recent priming. Therefore, MS is not only preceded by EBV infection, but also associated with broader EBV-specific TCR repertoires, consistent with an ongoing anti-EBV immune reaction in MS.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Tarbouriech2022,

title = {Borna Disease Virus 1 Phosphoprotein Forms a Tetramer and Interacts with Host Factors Involved in DNA Double-Strand Break Repair and mRNA Processing},

author = {Nicolas Tarbouriech and Florian Chenavier and Junna Kawasaki and Kamel Bachiri and Jean-Marie Bourhis and Pierre Legrand and Lily L. Freslon and Estelle M. N. Laurent and Elsa Suberbielle and Rob W. H. Ruigrok and Keizo Tomonaga and Daniel Gonzalez-Dunia and Masayuki Horie and Etienne Coyaud and Thibaut Crépin},

doi = {10.3390/v14112358},

issn = {1999-4915},

year  = {2022},

date = {2022-11-00},

urldate = {2022-11-00},

journal = {Viruses},

volume = {14},

number = {11},

publisher = {MDPI AG},

abstract = {<jats:p>Determining the structural organisation of viral replication complexes and unravelling the impact of infection on cellular homeostasis represent important challenges in virology. This may prove particularly useful when confronted with viruses that pose a significant threat to human health, that appear unique within their family, or for which knowledge is scarce. Among Mononegavirales, bornaviruses (family Bornaviridae) stand out due to their compact genomes and their nuclear localisation for replication. The recent recognition of the zoonotic potential of several orthobornaviruses has sparked a surge of interest in improving our knowledge on this viral family. In this work, we provide a complete analysis of the structural organisation of Borna disease virus 1 (BoDV-1) phosphoprotein (P), an important cofactor for polymerase activity. Using X-ray diffusion and diffraction experiments, we revealed that BoDV-1 P adopts a long coiled-coil α-helical structure split into two parts by an original β-strand twist motif, which is highly conserved across the members of whole Orthobornavirus genus and may regulate viral replication. In parallel, we used BioID to determine the proximal interactome of P in living cells. We confirmed previously known interactors and identified novel proteins linked to several biological processes such as DNA repair or mRNA metabolism. Altogether, our study provides important structure/function cues, which may improve our understanding of BoDV-1 pathogenesis.</jats:p>},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{C2022,

title = {Identification of bacterial lipopeptides as key players in IBS},

author = {Petitfils C, Maurel S, Payros G, Hueber A, Agaiz B, Gazzo G, Marrocco R, Auvray F, Langevin G, Motta JP, Floch P, Tremblay-Franco M, Galano JM, Guy A, Durand T, Lachambre S, Durbec A, Hussein H, Decraecker L, Bertrand-Michel J, Saoudi A, Oswald E, Poisbeau P, Dietrich G, Melchior C, Boeckxstaens G, Serino M, Le Faouder P, Cenac N.},

url = {https://pubmed.ncbi.nlm.nih.gov/36241390/},

doi = {10.1136/gutjnl-2022-328084},

year  = {2022},

date = {2022-10-14},

journal = {Gut},

keywords = {},

pubstate = {published},

tppubtype = {article}

}