MICROVUETMCIC-C1q EIA

The importance of circulating immune complexes (CIC) and their relationship to various diseases has been the subject of investigation for a number of years. Formation of immune complexes is a protective, ongoing, and usually benign, process of a normally functioning immune system. CIC are removed from the circulation in the normal host by a number of complex biochemical, enzymatic, and cellular processes. Key to the elimination of many CIC is the activation of the classical complement pathway. However, under certain disease conditions that are still poorly understood, immune complexes may initiate complement-dependent injury of various organs and tissues. This activation of complement may begin a series of potentially destructive events in the host including anaphylatoxin production, cell lysis, leukocyte stimulation, and activation of macrophages and other cells. When immune complexes become fixed to vessel walls or cell membranes, destruction of normal tissue can occur, as in some cases of glomerulonephritis. Certain properties of CIC influence their potential pathogenicity. Of particular importance are: (1) nature, size and concentration of the antigen; (2) nature, size and concentration of the antibody; and, (3) rate of formation and clearance of the immune complexes. Circulating immune complexes have been measured in a variety of conditions: infections, autoimmune disorders, trauma, and neoplastic proliferative diseases. Current studies suggest that CIC determination can be important in the evaluation of certain diseases and, sometimes, in monitoring efficiency of therapy. This is especially true in systemic lupus erythematosus (SLE) and some forms of rheumatoid arthritis (RA) . Classically, the first disease state linked to the formation of immune complexes was serum sickness, described in the early 1900’s by von Pirquet. Since that time elevated levels of CIC have been described in autoimmune diseases (SLE, SLE-related syndrome, RA), glomerulonephritis, neoplastic disease (Hodgkin’s, leukemia), bacterial infections (subacute bacterial endocarditis [SBE], leprosy), parasitic infections (malaria, schistosomiasis) and viral infections (hepatitis, mononucleosis) . Over 40 assay techniques have been described to detect or quantitate CIC. Such tests as the Raji Cell assay, C1q deviation test, conglutinin test, fluid phase C1q binding procedures, rheumatoid factor assay, PEG precipitin test, and solid phase C1q assays have been described. Since the size and physiochemical properties of CIC vary markedly, none of these assays has been accepted as a standard. A collaborative study sponsored by the World Health Organization in 1978 determined that no single method was appropriate in all suspected disease states and recommended that at least two different assay techniques be performed to detect and measure CIC adequately.