Complement receptor

A complement receptor is a membrane-bound receptor belonging to the complement system, which is part of the innate immune system. Complement receptors bind effector protein fragments that are produced in response to antigen-antibody complexes or damage-associated molecules.[1] Complement receptor activation contributes to the regulation of inflammation, leukocyte extravasation, and phagocytosis; it also contributes to the adaptive immune response.[2][3] Different complement receptors can participate in either the classical complement pathway, the alternative complement pathway, or both.[4]

Complement receptor
Identifiers
SymbolComplement receptor
Membranome116

Expression and function

White blood cells, particularly monocytes and macrophages, express complement receptors on their surface. All four complement receptors can bind to fragments of complement component 3 or complement component 4 coated on pathogen surface, but the receptors trigger different downstream activities.[1] Complement receptor (CR) 1, 3, and 4 function as opsonins which stimulate phagocytosis, whereas CR2 is expressed only on B cells as a co-receptor.

Red blood cells (RBCs) also express CR1, which enables RBCs to carry complement-bound antigen-antibody complexes to the liver and spleen for degradation.[5]

CR #NameMolecular weight (Da, approx.)[1]Ligand[4]CDMajor cell types[4]aMajor activities[1]
CR1Complement receptor 1190,000–250,000 C3b, C4b, iC3bCD35B, E, FDC, Mac, M0, PMN Immune complex transport (E); phagocytosis (PMN, Mac); immune adhesion (E); cofactor and decay-acceleration; secondary Epstein-Barr virus receptor
CR2Complement receptor 2145,000 C3d, iC3b, C3dg, Epstein-Barr virusCD21B, FDC B cell coactivator, primary Epstein-Barr virus receptor, CD23 receptor
CR3Macrophage-1 antigen or "integrin αMβ2"170,000 α chain + common 95,000 β chain iC3bCD11b+CD18FDC, Mac, M0, PMN Leukocyte adherence, phagocytosis of iC3b-bound particles
CR4Integrin alphaXbeta2 or "p150,95"150,000 α chain + common 95,000 β chain iC3bCD11c+CD18D, Mac, M0, PMN Leukocyte adhesion
C3AR1C3a receptor75,000 C3a-Endo, MC, Pha Cell activation
C5AR1C5a receptor50,000 C5aCD88Endo, MC, Pha Cell activation, immune polarization, chemotaxis
a.^ B: B cell. E: erythrocyte. Endo: endothelial cell. D: dendritic cell. FDC: follicular dendritic cell. Mac: macrophage. MC: mast cell. M0: monocyte. Pha: phagocyte. PMN: polymorphonuclear leukocyte.

Clinical significance
Main articles: Complement system § Role in disease, Classical complement pathway § Clinical significance, and Alternative complement pathway § Role in disease

Deficits in complement receptor expression can cause disease.[6] Mutations in complement receptors which alter receptor function can also increase risk of certain diseases.[1]

See also

References
  1. Holers VM (29 January 2014). "Complement and its receptors: new insights into human disease". Annual Review of Immunology. 32: 433–59. doi:10.1146/annurev-immunol-032713-120154. PMID 24499275.
  2. Verschoor A, Kemper C, Köhl J (15 September 2017). "Complement Receptors". eLS: 1–17. doi:10.1002/9780470015902.a0000512.pub3. ISBN 9780470015902.
  3. Carroll MC (December 2008). "Complement and humoral immunity". Vaccine. 26 Suppl 8 (Suppl 8): I28-33. doi:10.1016/j.vaccine.2008.11.022. PMC 4018718. PMID 19388161.
  4. Janeway Jr CA, Travers P, Walport M, Shlomchik MJ (2001). "The complement system and innate immunity". Immunobiology: The Immune System in Health and Disease (5th ed.). New York: Garland Science. Retrieved 17 June 2020.
  5. Parham P (2005). The Immune System (2nd ed.). Garland Science. ISBN 9780815340935.
  6. Schwartz RA, Thomas I. "Complement Receptor Deficiency: eMedicine Dermatology". Medscape. Retrieved 7 December 2010.
This article is issued from Wikipedia. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.