title: Prevention of autoimmunity and control of recall response to exogenous antigen by Fas death receptor ligand expression on T cells.
abstract: Mice with mutations in the gene encoding Fas ligand (FasL) develop lymphoproliferation and systemic autoimmune diseases. However, the cellular subset responsible for the prevention of autoimmunity in FasL-deficient mice remains undetermined. Here, we show that mice with FasL loss on either B or T cells had identical life span as littermates, and both genotypes developed signs of autoimmunity. In addition, we show that T cell-dependent death was vital for the elimination of aberrant T cells and for controlling the numbers of B cells and dendritic cells that dampen autoimmune responses. Furthermore, we show that the loss of FasL on T cells affected the follicular dentritic cell network in the germinal centers, leading to an impaired recall response to exogenous antigen. These results disclose the distinct roles of cellular subsets in FasL-dependent control of autoimmunity and provide further insight into the role of FasL in humoral immunity.
authors.affiliation: INSERM U580, Université Paris Descartes, Hopital Necker, 161 rue de Sèvres 75015 Paris, France.
authors.forename: Imed
authors.initials: I
authors.lastname: Mabrouk
authors.forename: Stéphanie
authors.initials: S
authors.lastname: Buart
authors.forename: Meriem
authors.initials: M
authors.lastname: Hasmim
authors.forename: Christelle
authors.initials: C
authors.lastname: Michiels
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Connault
authors.forename: Paule
authors.initials: P
authors.lastname: Opolon
authors.forename: Gilles
authors.initials: G
authors.lastname: Chiocchia
authors.forename: Matthieu
authors.initials: M
authors.lastname: Lévi-Strauss
authors.forename: Salem
authors.initials: S
authors.lastname: Chouaib
authors.forename: Saoussen
authors.initials: S
authors.lastname: Karray
mesh_terms: D000818:Animals; D000941:Antigens / Q000276:immunology; D001327:Autoimmune Diseases / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D001402:B-Lymphocytes / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D003713:Dendritic Cells / Q000276:immunology* / Q000378:metabolism; D053222:Fas Ligand Protein / Q000235:genetics / Q000276:immunology*; D008206:Lymphatic Diseases / Q000235:genetics / Q000276:immunology / Q000473:pathology; D051379:Mice; D018345:Mice, Knockout; D013601:T-Lymphocytes / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D019014:fas Receptor / Q000276:immunology / Q000378:metabolism
chemical_list: D000941:Antigens; D053222:Fas Ligand Protein; C491899:Fas protein, mouse; D019014:fas Receptor