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 the 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) it 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.⁶

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.⁷

Known levels of Factor H aid in the diagnosis of several disease states such as atypical Hemolytic-Uremic Syndrome (aHUS), age-related macular degeneration, and dense deposit disease. 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, and as a camouflage to tumor cells for protection against the host immune system. This broad range of testing gives Factor H an appeal to many types of research.⁹