Not always the bad guys: B cells as regulators of autoimmune pathology.
When B cells react aggressively against self, the potential for pathology is extreme. It is therefore not surprising that B-cell depletion is seen as an attractive therapy in autoimmune diseases. However, B cells can also be essential for restraining unwanted autoaggressive T-cell responses. Recent advances have pointed to interleukin-10 (IL-10) production as a key component in B-cell-mediated immune regulation. In this Opinion article, we develop a hypothesis that triggering of Toll-like receptors controls the propensity of B cells for IL-10 production and immune suppression. According to this model, B cells can translate exposure to certain microbial infections into protection from chronic inflammatory diseases.
Fillatreau
Simon
S
Simon Fillatreau is at the Immune regulation group, Deutsches Rheuma-ForschungsZentrum, Charitéplatz 1, 10117 Berlin, Germany.
Gray
David
D
Anderton
Stephen M
SM
D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology* / Q000473:pathology; D001402:B-Lymphocytes / Q000276:immunology*; D019013:CD40 Antigens / Q000276:immunology / Q000378:metabolism; D003141:Communicable Diseases / Q000276:immunology / Q000473:pathology; D006801:Humans; D007110:Immunity, Active; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D016753:Interleukin-10 / Q000096:biosynthesis; D008213:Lymphocyte Activation; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D051193:Toll-Like Receptors / Q000276:immunology / Q000378:metabolism
D019013:CD40 Antigens; D051193:Toll-Like Receptors; D016753:Interleukin-10