Complement and immune complex diseases.

Research during the past decade has led to a much greater understanding of the activation and control, as well as a more complete delineation, of the complement system of proteins. There has been definition of the roles of individual components in modulation of immune complex formation, the deposition of which leads to tissue injury in the autoimmune connective tissue diseases. The ability of serum to render immune complexes more soluble is complement-mediated and appears to be an important protective mechanism against immune complex diseases. Inherited deficiencies and production of non-functional variants of complement components, decreased synthesis, hypercatabolism, and the presence of serum inhibitors may all contribute to the reduced immune complex solubilisation which has been found in the connective tissue diseases. More work is required to define further the role of complement and immune complexes in the basic pathogenesis of these diseases.