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International Immunology Advance Access originally published online on October 11, 2004
International Immunology 2004 16(12):1685-1690; doi:10.1093/intimm/dxh159
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© 2004 The Japanese Society for Immunology

Antigen localization within the splenic marginal zone restores humoral immune response and IgG class switch in complement C4-deficient mice

Berit Zachrau1, Doreen Finke1, Katja Kropf1, Hans-Juergen Gosink2, Holger Kirchner1 and Siegfried Goerg1

1 Institute for Immunology and Transfusion Medicine and 2 Department of Radiotherapy and Nuclear Medicine, Medical University of Luebeck, Ratzeburger Allee 160, D-23560 Luebeck, Germany

Correspondence to: S. Goerg; E-mail: goerg{at}immu.mu-luebeck.de

Defects of early complement components (C1, C4 and C2) are associated with the development of systemic lupus erythematosus (SLE). The availability of complement knockout mice has increased our knowledge on the role of complement in the regulation of adaptive immunity. An impaired removal of apoptotic bodies, a disturbed clearance of IgG immune complexes (ICs) and an insufficient B-cell regulation via complement receptors CD21/CD35 have been discussed as explanations for the induction of autoimmunity; however, a unifying hypothesis for the loss of B-cell tolerance in the absence of C1 or C4 is still lacking. Using IgM-containing ICs, we observed a significant accumulation of antigen within the splenic marginal zone (MZ) of C4-deficient mice but not in C3-deficient or complement receptors CD21/CD35-deficient mice. The targeting of antigen toward the MZ restored adaptive immunity (antibody response and class switch) in C4-deficient animals. A new explanation for the association of SLE and complement C4 deficiency would be that in the absence of C4, natural antibodies (IgM type) localize more self-antigen toward the MZ so that the auto-antibody response is increased and autoimmune disease ensues. As such, an inadequate localization of self-antigens might be responsible for the annulment of peripheral B-cell tolerance in the absence of C4.

Keywords: B cells, complement, immune complexes, marginal zone

Transmitting editor: D. T. Fearon


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