Anti-Human iC3b/C3dg/C3d Monoclonal Antibody (clone C3-12.2) -0.5 mg (CAT#: CB-P293-AB) Datasheet

Antibody

Antibody clone C3-12.2 recognizes complement iC3b, C3dg and C3d. The recognition domain is determined as CUB-TED. The antibody blocks C3 activation by AP C3 convertase. The complement system plays an important role in both innate and adaptive immune responses, and can produce inflammatory and protective responses to pathogen attacks before the adaptive response occurs. It consists of a complex family of proteins and receptors, which are present in the circulatory system, tissues and other body fluids. There are three ways to activate complement. The classical pathway is triggered by immune complexes. The lectin pathway through surface-bound lectins; and all surfaces that are not specifically protected. Each produces C3 convertase, a serine protease that cleaves the central complement protein C3 and produces the main cleavage fragment C3b. C3 and C5 invertases are enzyme complexes that initiate and amplify the activity of the complement pathway and ultimately produce cytolytic MAC. The synthesis of C3 is tissue-specific and is regulated in response to a variety of stimulants. After being cleaved by C3 convertase, toxin C3a and activating C3b are formed. When bound to the cell surface, C3b forms the start of the terminal complement pathway by initiating the formation of C5 convertase. The molecular weight of C3 is app. 185kDa is the most abundant protein in the complement system, and the serum protein level is about 1.3 mg/ml. C3 is mainly produced by the liver, but can also be produced in macrophages, neutrophils, endothelial and epithelial cells. Due to the high level of circulation and low bioreactivity, C 3 can act in a fast and effective manner when dangers such as the following occur. Encountered pathogens. C3 deficiency may be detrimental to the host, leading to repeated infections or autoimmune diseases. Although rare, C3 deficiency has been reported. These patients suffer from repeated infections such as Streptococcus pneumoniae or Neisseria meningitidis due to lack of opsonization, and the development of DC and Treg is impaired. The polymorphism in C3 is related to AMD and aHUS. In addition to removing pathogens, C3 is also important in removing circulating immune complexes by assisting the phagocytic ability of macrophages. Abnormal functions of this system can lead to the development of autoimmune diseases and replenish deposits in the tissues.

Infectious diseases, Nephrology