title: Intrinsic Toll-like receptor signalling drives regulatory function in B cells.
abstract: B cells can contribute to immunity through production of antibodies, presentation of antigen to T cells, and secretion of cytokines. B cell activation can result in various outcomes for the host. In general B cell responses are beneficial during infections, and deleterious during autoimmune diseases. However, B cells can also limit host defence against pathogens, and protect from autoimmune pathologies. B cells can therefore act both as drivers and as regulators of immunity. Understanding how these opposite functions are mediated shall stimulate the elaboration of novel approaches for manipulating the immune system. B cells might acquire distinct functional properties depending on their mode of activation. Antigen-specific B cell responses require triggering of B cell receptor (BCR) by antigen, and provision of helper signals by T cells. B cells also express various innate immune receptors, and can directly respond to microbial products. Here, we discuss how intrinsic signalling via Toll-like receptors contributes to the suppressive functions of B cells during autoimmune and infectious diseases.
authors.affiliation: Immune regulation group, Deutsche Rheuma-Forschungszentrum, a Leibniz institute, Chariteplatz 1, 10117 Berlin, Germany.
authors.forename: Ping
authors.initials: P
authors.lastname: Shen
authors.forename: Vicky
authors.initials: V
authors.lastname: Lampropoulou
authors.forename: Ulrik
authors.initials: U
authors.lastname: Stervbo
authors.forename: Ellen
authors.initials: E
authors.lastname: Hilgenberg
authors.forename: Stefanie
authors.initials: S
authors.lastname: Ries
authors.forename: Aurelie
authors.initials: A
authors.lastname: Mecqinion
authors.forename: Simon
authors.initials: S
authors.lastname: Fillatreau
mesh_terms: D001402:B-Lymphocytes / Q000276:immunology / Q000378:metabolism*; D003141:Communicable Diseases / Q000276:immunology*; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology*; D006801:Humans; D015398:Signal Transduction / Q000276:immunology*; D051193:Toll-Like Receptors / Q000276:immunology / Q000378:metabolism*
chemical_list: D051193:Toll-Like Receptors