Journal of Leukocyte Biology Myeloid cells, immune suppression, tumor immunology
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(Journal of Leukocyte Biology. 2002;72:249-261.)
© 2002 by Society for Leukocyte Biology

Complement’s participation in acquired immunity

Claus Henrik Nielsen* and Robert Graham Quinton Leslie{dagger}

* Institute for Inflammation Research, Rigshospitalet, University Hospital Copenhagen; and
{dagger} Department of Immunology and Microbiology, University of Southern Denmark, Odense

Correspondence: Graham Leslie, Associate Professor, Ph.D., Department of Immunology and Microbiology, Institute of Medical Biology, University of Southern Denmark (Odense), Winsløwparken 21-I, 5000 Odense C, Denmark. E-mail: gleslie{at}health.sdu.dk

The preliminary evidence for the involvement of complement in promoting primary humoral responses dates back over a quarter of a century. However, it is only in the course of the past decade or so that the detailed mechanisms underlying complement’s influence have been characterized in depth. It is now clear that complement serves as a regulator of several B cell functions, including specific antibody production, antigen uptake, processing and presentation, and shaping of the B cell repertoire. Of key importance, in this respect, is the role played by the B cell-signaling triad consisting of the B cell receptor for antigen (BCR), a complex composed of the iC3b/C3d fragment-binding complement type 2 receptor (CR2, CD21) and its signaling element CD19 and the IgG-binding receptor Fc{gamma}RIIb (CD32). The positive or negative outcome of signaling through this triad is determined by the context in which antigen is seen, be it alone or in association with natural or induced antibodies and/or C3-complement fragments. The aim of this review is to describe the present status of our understanding of complement’s participation in acquired immunity and the regulation of autoimmune responses.

Key Words: B cell receptor • follicular dendritic cells • classical pathway • immune complexes




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