Immune-complex vasculitis: role of complement and IgG-Fc receptor functions

Vasculitis contributes a major component to the pathogenesis of rheumatic diseases and glomerulonephritis. A common feature of these diseases is the presence of serum immune complexes (IC) which may be deposited in blood vessel walls. The modification of the size and solubility of IC by the classical and alternative complement pathways, and the recent demonstration of the role of cellular complement receptors and IgG-Fc receptors in the handling of IC, now allow a better understanding of the pathogenesis of the severe forms of vasculitis. When complement deficiencies are present, the handling of IC is impaired, and vasculitis results. New blood tests for Factor VIII-related antigen, alkaline ribonuclease, plasma thrombospondin, and anti-neutrophil cytoplasmic antibody correlate with the presence of selected types of vasculitis. In addition, tissue thromboplastin release after application of defined tourniquet pressure can also detect subtle blood vessel injury. These new tests may allow diagnosis without risky organ biopsies. Advances in the diagnosis and treatment of vasculitis will also be discussed.