MICROVUETMFactor H EIA

The alternative complement pathway provides innate protection against microbial agents in the absence of specific antibody. The activation of this complement pathway can be triggered by a variety of substances including microbial polysaccharides or lipids, gram negative bacterial lipopolysaccharides, and surface determinants present on some viruses, parasites, virally infected mammalian cells, and cancer cells. In autoimmune diseases, the alternative complement pathway may contribute directly to tissue damage. Factor H is involved in the regulation of the alternative pathway of complement. In blood, activation of C3, under normal conditions, is kept at a low level by control proteins, Factor H and Factor I. Factor H functions in two ways to inactivate the C3bBb enzyme: 1) it accelerates the dissociation of Bb from C3b; and 2) serves as a cofactor for Factor I, a serine protease, which cleaves C3b into iC3b, which can no longer form the C3 convertase with Factor B. Factor H also regulates the spontaneous fluid-phase activation of the alternative complement pathway by C3b like forms of C3 that continuously arise in plasma and serum. Therefore, when concentrations of Factor H fall below normal levels, there is rapid fluid-phase activation and consumption of complement components both in vivo and in vitro. Factor H is a single-chain glycoprotein with a molecular weight of 150 KD.7 Concentrations found in normal human plasma/serum is approximately 500 μg/mL, although it can range from 116-562 μg/mL depending on multiple factors (environment and genetic) . Factor H regulates complement activation on the cellular surface and in fluid phase while participating in roles for both the alternative and classical pathways. The majority of Factor H is produced in the liver. However, it can also be expressed locally by endothelial cells, epithelial cells, platelets, mesenchymal stem cells, among others. Complement Factor H has been implicated in the research of many autoimmune diseases. Studies have included using Factor H as a serum biomarker of multiple sclerosis disease state, as a therapy for renal diseases associated with Factor H abnormalities, as a camouflage to tumor cells for protection against the host immune system, and in clarification surrounding disease states such as atypical Hemolytic-Uremic Syndrome (aHUS), age-related macular degeneration, and dense deposit disease. This broad range of testing gives Factor H an appeal to many types of research.