Complement factors and breakdown products acting through cell surface membrane receptors block the differentiation of human B lymphocytes into immunoglobulin secreting cells. Complement receptors are associated with B cell surface immunoglobulin under certain circumstances. Furthermore, complement receptor expression is cell-cycle dependent. Monovalent ligands inhibit while polyvalent enhance the anti-IgM induced human B cell increase in intracytoplasmic calcium ion concentration and cell proliferation. Understanding of the mechanism of regulation of immune responses by complement and the role of complement receptors on human B cells is crucial for the understanding of the immunopathogenesis of autoimmune diseases since they are frequently associated with complement activation, depression of complement factor levels and changes in complement receptors.
