Abstract
For more than 30 years it has been known that complement plays a central role in the development of humoral immune responses. Today it is clear that complement influences a variety of B cell functions, including the uptake,processing and presentation of foreign and selfantigens,the production of specific antibodies as well as shaping of the B cell repertoire. A central role in the performance of these functions is played by the B cell signalling triad consisting of the B cell receptor for antigen(BCR), a complex consisting of the iC3b/C3d fragmentbinding complement type 2 receptor (CR2, CD21) and its signalling element, CD19, and the IgG-binding receptor,Fc?RIIb (CD32). Recent evidence suggests that complement,in addition to facilitating the uptake and presentation of antigen to T helper cells by antigen-presenting cells, also regulates T cell functions by promoting the production of the pro-inflammatory cytokines TNF-a and IFN-? on the one hand, and the differentiation of regulatory T cells producing IL-10 on the other. This review aims at describing the present status of our understanding of the mechanisms underlying complement regulation of acquired immunity and autoimmunity.