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Complement C2 is a protein that in humans is encoded by the C2gene.[5] The protein encoded by this gene is part of the classical pathway of the complement system, acting as a multi-domain serine protease. Deficiency of C2 has been associated with certain autoimmune diseases.[5]
The Complement system is generated to regulate self protection from infection. The overall Complement system is composed of protein groups that collaborate in destroying foreign invaders, which ultimately remove debris from cells and tissues. When the body detects a foreign invader, the body signals the Complement system and the Complement component 2 protein attaches to Complement system 4 resulting in an immune response. Complement component 2 protein is critical for regulating the body's immune response. The C2 nerves carry messages to muscles involved in neck flexion.
Function
In the classical and lectin pathways of complement activation, formation of the C3-convertase and C5-convertases requires binding of C2 to an activated surface-bound C4b in the presence of Mg2+; the resultant C4bC2 complex is cleaved by C1s or MASP2 into C2a and C2b. It is thought that cleavage of C2 by C1s, while bound to C4b, results in a conformational rotation of C2b whereas the released C2a fragment may retain most of its original structure.
C2b is the smallest , enzymatically active, fragment of C3 convertase in this pathway, C4b2b (NB: some sources now refer to the larger fragment of C2 as C2b, making the C3 convertase C4b2b, whereas older sources refer to the larger fragment of C2 as C2a, making the C3 convertase C4b2a). The smaller fragment, C2a (or C2b, depending on the source) is released into the fluid phase.[6]
^Sjöholm AG, Jönsson G, Braconier JH, Sturfelt G, Truedsson L (January 2006). "Complement deficiency and disease: an update". Molecular Immunology. 43 (1–2): 78–85. doi:10.1016/j.molimm.2005.06.025. PMID16026838.
^Wen L, Atkinson JP, Giclas PC (April 2004). "Clinical and laboratory evaluation of complement deficiency". The Journal of Allergy and Clinical Immunology. 113 (4): 585–93, quiz 594. doi:10.1016/j.jaci.2004.02.003. PMID15100659.
Further reading
Bartholomew WR, Shanahan TC (1991). "Complement components and receptors: deficiencies and disease associations". Immunology Series. 52: 33–51. PMID2091785.
Horiuchi T, Macon KJ, Kidd VJ, Volanakis JE (Mar 1989). "cDNA cloning and expression of human complement component C2". Journal of Immunology. 142 (6): 2105–2111. PMID2493504.
Cole FS, Whitehead AS, Auerbach HS, Lint T, Zeitz HJ, Kilbridge P, Colten HR (Jul 1985). "The molecular basis for genetic deficiency of the second component of human complement". The New England Journal of Medicine. 313 (1): 11–16. doi:10.1056/NEJM198507043130103. PMID2582254.
Wu LC, Morley BJ, Campbell RD (Jan 1987). "Cell-specific expression of the human complement protein factor B gene: evidence for the role of two distinct 5'-flanking elements". Cell. 48 (2): 331–342. doi:10.1016/0092-8674(87)90436-3. PMID3643061. S2CID32752642.
Liu CC, Ahearn JM (2007). "Chap. 13: Complement and systemic lupus erythematosus". In Wallace DJ, Hahn BH (eds.). Dubois’ Lupus Erythematosus (7th ed.). Philadelphia: Lippincott Williams & Wilkins. pp. 214–235.
Ippolito A, Wallace DJ, Gladman D, Fortin PR, Urowitz M, Werth V, et al. (March 2011). "Autoantibodies in systemic lupus erythematosus: comparison of historical and current assessment of seropositivity". Lupus. 20 (3): 250–255. doi:10.1177/0961203310385738. PMID21362750.
