INSTRUCTIONS FOR USE BINDAZYME Human Anti-C1q Enzyme Immunoassay Kit MK079

Activation of the classical pathway of the complement system follows binding of complement C1q (C1q) by immune complexes, acute phase proteins, apoptotic cells and cell debris. An inadequacy in the removal of apoptotic cells/material has been implicated in the aetiopathogenesis of SLE. Indeed, inherited deficiencies in C1q, are invariably associated with a severe, lupus-like disease that appears early in life. Autoantibodies to C1q could also result in reduced C1q activity, so an association of such antibodies with SLE compared to other connective tissue diseases is not unexpected. Furthermore, cross-sectional studies report an incidence in SLE of anti-C1q antibodies of between 30-40%, rising to between 60-100% for patients with associated renal disease. High levels of antibody to C1q alone however, are not sufficient to cause renal disease as demonstrated in patients with hypocomplementemic urticarial vasculitis (HUVS): a rare presentation of systemic lupus erythematosus.