Monoclonal antibody 1A2 recognizes mouse complement factor H (CFH). CFH is the first regulatory protein of the alternative pathway of the complement system. There are three pathways for complement activation; the classical pathway, the alternative pathway and the lectin activation pathway. These pathways converge to form The C3/C5 convertase that produces C3a, C3b, C5a and C5b has considerable biological activity. Supplementary regulators are necessary to prevent the harmful production of these mediators and potential damage to their own tissues. Cell membrane protein complement receptors 1 (CR1; CD35), decay accelerating factor (CD55) and membrane cofactor protein (CD46) are all members of the complement activation family of regulators. These proteins give C3b and/or C4b to them to accelerate the inherent decay of C3/C5 convertase And/or the ability element factor I (CFI) for the cleavage and inactivation (i) of C3b and C4b as a coenzyme.
Genetic human analysis reveals a clear association between CFH and different human diseases. These diseases include kidney disease, atypical forms of hemolytic-uremic syndrome (aHUS) and membranous proliferative glomerulonephritis (MPGN). Moreover, CFH is associated with age-related macular degeneration (AMD), which is an eye disease.