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Fcγ RIIB and autoimmunity
Author(s) -
Espéli Marion,
Smith Kenneth G. C.,
Clatworthy Menna R.
Publication year - 2016
Publication title -
immunological reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.839
H-Index - 223
eISSN - 1600-065X
pISSN - 0105-2896
DOI - 10.1111/imr.12368
Subject(s) - autoimmunity , immunology , immune system , acquired immune system , biology , innate immune system , germinal center , autoantibody , complement system , complement receptor , classical complement pathway , receptor , microbiology and biotechnology , b cell , antibody , biochemistry
Summary Autoimmune diseases are characterized by adaptive immune responses against self‐antigens, including humoral responses resulting in the production of autoantibodies. Autoantibodies generate inflammation by activating complement and engaging Fcγ receptors (FcγRs). The inhibitory receptor Fcγ RIIB plays a central role in regulating the generation of autoantibodies and their effector functions, which include activation of innate immune cells and the cellular arm of the adaptive immune system, via effects on antigen presentation to CD 4 T cells. Polymorphisms in Fcγ RIIB have been associated with susceptibility to autoimmunity but protection against infections in humans and mice. In the last few years, new mechanisms by which Fcγ RIIB controls the adaptive immune response have been described. Notably, Fcγ RIIB has been shown to regulate germinal center B cells and dendritic cell migration, with potential impact on the development of autoimmune diseases. Recent work has also highlighted the implication of Fcγ RIIB on the regulation of the innate immune system, via inhibition of Toll‐like receptor‐ and complement receptor‐mediated activation. This review will provide an update on the role of Fcγ RIIB in adaptive immune responses in autoimmunity, and then focus on their emerging function in innate immunity.