@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}

}

@article{36165182,

title = {IgG Subclass-Dependent Pulmonary Antigen Retention during Acute IgG-Dependent Systemic Anaphylaxis in Mice.},

author = {Todorova B and Godon O and Conde E and Gillis CM and Iannascoli B and Richard-Le Goff O and Fiole D and Roumenina LT and Leusen JHW and Murphy AJ and Macdonald LE and Reber LL and Jönsson F and Bruhns P},

url = {https://pubmed.ncbi.nlm.nih.gov/36165182/},

doi = {10.4049/jimmunol.2200234},

year  = {2022},

date = {2022-10-01},

journal = {J Immunol},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{vanJoost.2022,

title = {IL-2 and IL-15 drive intrathymic development of distinct periphery-seeding CD4+Foxp3+ regulatory T lymphocytes},

author = {Cécile Apert and Ariel Galindo-Albarrán and Sarah Castan and Claire Detraves and Héloise Michaud and Nicola McJannett and Bart Haegeman and Simon Fillatreau and Bernard Malissen and Georg Hollander and Saulius Zuklys and Jérémy Santamaria and Olivier Joffre and Paola Romagnoli and Joost van Meerwijk},

url = {https://www.frontiersin.org/articles/10.3389/fimmu.2022.965303/full},

doi = {10.3389/fimmu.2022.965303},

year  = {2022},

date = {2022-09-08},

journal = {Frontiers in Immunology},

abstract = {Development of Foxp3-expressing regulatory T-lymphocytes (Treg) in the thymus is controlled by signals delivered in T-cell precursors via the TCR, co-stimulatory receptors, and cytokine receptors. In absence of IL-2, IL-15 or their receptors, fewer Treg apparently develop in the thymus. However, it was recently shown that a substantial part of thymic Treg are cells that had recirculated from the periphery back to the thymus, troubling interpretation of these results. We therefore reassessed the involvement of IL-2 and IL-15 in the development of Treg, taking into account Treg-recirculation. At the age of three weeks, when in wt and IL-15-deficient (but not in IL-2-deficient) mice substantial amounts of recirculating Treg are present in the thymus, we found similarly reduced proportions of newly developed Treg in absence of IL-2 or IL-15, and in absence of both cytokines even less Treg developed. In neonates, when practically no recirculating Treg were found in the thymus, the absence of IL-2 led to substantially more reduced Treg-development than deficiency in IL-15. IL-2 but not IL-15 modulated the CD25, GITR, OX40, and CD73-phenotypes of the thymus-egress-competent and periphery-seeding Treg-population. Interestingly, IL-2 and IL-15 also modulated the TCR-repertoire expressed by developing Treg. Upon transfer into Treg-less Foxp3sf mice, newly developed Treg from IL-2- (and to a much lesser extent IL-15-) deficient mice suppressed immunopathology less efficiently than wt Treg. Taken together, our results firmly establish important non-redundant quantitative and qualitative roles for IL-2 and, to a lesser extent, IL-15 in intrathymic Treg-development.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Bergamelli2022,

title = {Human Cytomegalovirus Modifies Placental Small Extracellular Vesicle Composition to Enhance Infection of Fetal Neural Cells In Vitro},

author = {Mathilde Bergamelli and Hélène Martin and Yann Aubert and Jean-Michel Mansuy and Marlène Marcellin and Odile Burlet-Schiltz and Ilse Hurbain and Graça Raposo and Jacques Izopet and Thierry Fournier and Alexandra Benchoua and Mélinda Bénard and Marion Groussolles and Géraldine Cartron and Yann Tanguy Le Gac and Nathalie Moinard and Gisela D’Angelo and Cécile E. Malnou},

doi = {10.3390/v14092030},

issn = {1999-4915},

year  = {2022},

date = {2022-09-00},

urldate = {2022-09-00},

journal = {Viruses},

volume = {14},

number = {9},

publisher = {MDPI AG},

abstract = {<jats:p>Although placental small extracellular vesicles (sEVs) are extensively studied in the context of pregnancy, little is known about their role during viral congenital infection, especially at the beginning of pregnancy. In this study, we examined the consequences of human cytomegalovirus (hCMV) infection on sEVs production, composition, and function using an immortalized human cytotrophoblast cell line derived from first trimester placenta. By combining complementary approaches of biochemistry, electron microscopy, and quantitative proteomic analysis, we showed that hCMV infection increases the yield of sEVs produced by cytotrophoblasts and modifies their protein content towards a potential proviral phenotype. We further demonstrate that sEVs secreted by hCMV-infected cytotrophoblasts potentiate infection in naive recipient cells of fetal origin, including human neural stem cells. Importantly, these functional consequences are also observed with sEVs prepared from an ex vivo model of infected histocultures from early placenta. Based on these findings, we propose that placental sEVs could be important actors favoring viral dissemination to the fetal brain during hCMV congenital infection.</jats:p>},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid35644112,

title = {Tissue-resident CD8 T cells in central nervous system inflammatory diseases: present at the crime scene and …guilty},

author = {Doron Merkler and Ilena Vincenti and Frederick Masson and Roland S Liblau},

doi = {10.1016/j.coi.2022.102211},

issn = {1879-0372},

year  = {2022},

date = {2022-08-01},

urldate = {2022-08-01},

journal = {Curr Opin Immunol},

volume = {77},

pages = {102211},

abstract = {Tissue-resident memory T cells (T) represent a subset of antigen-experienced T cells that are constantly retained in a given tissue with limited trafficking through the circulation. These cells are characterized by expression of molecules enabling their tissue anchoring and downregulation of molecules promoting tissue egress. They reside at sites of previous antigen encounter and their number increases with age. T have been shown to provide rapid and efficient protection against tissue reinfection and T density correlates with efficient antitumor responses. Intriguingly, the density of CD8 T is increased in the central nervous system (CNS) of patients with neuroinflammatory diseases such as multiple sclerosis, or suffering from neurodegenerative diseases. In this review, we discuss current knowledge regarding the diversity of CNS-resident CD8 T cells and their role in CNS autoimmunity. Given their likely contribution to the protracted course of several inflammatory diseases of the CNS, their therapeutic targeting becomes an important challenge.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Martin2022b,

title = {Usutu Virus Infects Human Placental Explants and Induces Congenital Defects in Mice},

author = {Hélène Martin and Jonathan Barthelemy and Yamileth Chin and Mathilde Bergamelli and Nathalie Moinard and Géraldine Cartron and Yann Tanguy Le Gac and Cécile E. Malnou and Yannick Simonin},

doi = {10.3390/v14081619},

issn = {1999-4915},

year  = {2022},

date = {2022-08-00},

urldate = {2022-08-00},

journal = {Viruses},

volume = {14},

number = {8},

publisher = {MDPI AG},

abstract = {<jats:p>Usutu virus (USUV) is a neurotropic mosquito-borne flavivirus that has dispersed quickly in Europe these past years. This arbovirus mainly follows an enzootic cycle involving mosquitoes and birds, but can also infect other mammals, causing notably sporadic cases in humans. Although it is mainly asymptomatic or responsible for mild clinical symptoms, USUV has been associated with neurological disorders, such as encephalitis and meningoencephalitis, highlighting the potential health threat of this virus. Among the different transmission routes described for other flaviviruses, the capacity for some of them to be transmitted vertically has been demonstrated, notably for Zika virus or West Nile virus, which are closely related to USUV. To evaluate the ability of USUV to replicate in the placenta and gain access to the fetus, we combined the use of several trophoblast model cell lines, ex vivo human placental explant cultures from first and third trimester of pregnancy, and in vivo USUV-infected pregnant mice. Our data demonstrate that human placental cells and tissues are permissive to USUV replication, and suggest that viral transmission can occur in mice during gestation. Hence, our observations suggest that USUV could be efficiently transmitted by the vertical route.</jats:p>},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{2022,

title = {Quelle est la réalité des infections humaines par les Bornavirus ?},

doi = {10.1684/vir.2022.0965},

issn = {1267-8694},

year  = {2022},

date = {2022-07-01},

urldate = {2022-07-01},

journal = {Virologie},

volume = {26},

number = {4},

pages = {275--281},

publisher = {John Libbey Eurotext},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid35552381b,

title = {Influenza vaccination induces autoimmunity against orexinergic neurons in a mouse model for narcolepsy},

author = {Raphaël Bernard-Valnet and David Frieser and Xuan Hung Nguyen and Leila Khajavi and Clémence Quériault and Sébastien Arthaud and Silvia Melzi and Maxime Fusade-Boyer and Frederick Masson and Matthias Zytnicki and Abdelhadi Saoudi and Yves Dauvilliers and Christelle Peyron and Jan Bauer and Roland S Liblau},

doi = {10.1093/brain/awab455},

issn = {1460-2156},

year  = {2022},

date = {2022-06-01},

urldate = {2022-06-01},

journal = {Brain},

volume = {145},

number = {6},

pages = {2018--2030},

abstract = {Narcolepsy with cataplexy or narcolepsy type 1 is a disabling chronic sleep disorder resulting from the destruction of orexinergic neurons in the hypothalamus. The tight association of narcolepsy with HLA-DQB1*06:02 strongly suggest an autoimmune origin to this disease. Furthermore, converging epidemiological studies have identified an increased incidence for narcolepsy in Europe following Pandemrix® vaccination against the 2009-2010 pandemic 'influenza' virus strain. The potential immunological link between the Pandemrix® vaccination and narcolepsy remains, however, unknown. Deciphering these mechanisms may reveal pathways potentially at play in most cases of narcolepsy. Here, we developed a mouse model allowing to track and study the T-cell response against 'influenza' virus haemagglutinin, which was selectively expressed in the orexinergic neurons as a new self-antigen. Pandemrix® vaccination in this mouse model resulted in hypothalamic inflammation and selective destruction of orexin-producing neurons. Further investigations on the relative contribution of T-cell subsets in this process revealed that haemagglutinin-specific CD4 T cells were necessary for the development of hypothalamic inflammation, but insufficient for killing orexinergic neurons. Conversely, haemagglutinin-specific CD8 T cells could not initiate inflammation but were the effectors of the destruction of orexinergic neurons. Additional studies revealed pathways potentially involved in the disease process. Notably, the interferon-γ pathway was proven essential, as interferon-γ-deficient CD8 T cells were unable to elicit the loss of orexinergic neurons. Our work demonstrates that an immunopathological process mimicking narcolepsy can be elicited by immune cross-reactivity between a vaccine antigen and a neuronal self-antigen. This process relies on a synergy between autoreactive CD4 and CD8 T cells for disease development. This work furthers our understanding of the mechanisms and pathways potentially involved in the development of a neurological side effect due to a vaccine and, likely, to narcolepsy in general.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}