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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 | |
| Symbol | Complement receptor |
| Membranome | 116 |
Expression and function
editWhite 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 # | Name | Molecular weight (Da, approx.)[1] | Ligand[4] | CD | Major cell types[4]a | Major activities[1] |
|---|---|---|---|---|---|---|
| CR1 | Complement receptor 1 | 190,000–250,000 | C3b, C4b, iC3b | CD35 | B, E, FDC, Mac, M0, PMN | Immune complex transport (E); phagocytosis (PMN, Mac); immune adhesion (E); cofactor and decay-acceleration; secondary Epstein-Barr virus receptor |
| CR2 | Complement receptor 2 | 145,000 | C3d, iC3b, C3dg, Epstein-Barr virus | CD21 | B, FDC | B cell coactivator, primary Epstein-Barr virus receptor, CD23 receptor |
| CR3 | Macrophage-1 antigen or "integrin αMβ2" | 170,000 α chain common 95,000 β chain | iC3b | CD11b CD18 | FDC, Mac, M0, PMN | Leukocyte adherence, phagocytosis of iC3b-bound particles |
| CR4 | Integrin alphaXbeta2 or "p150,95" | 150,000 α chain common 95,000 β chain | iC3b | CD11c CD18 | D, Mac, M0, PMN | Leukocyte adhesion |
| C3AR1 | C3a receptor | 75,000 | C3a | – | Endo, MC, Pha | Cell activation |
| C5AR1 | C5a receptor | 50,000 | C5a | CD88 | Endo, MC, Pha | Cell activation, immune polarization, chemotaxis |
| C5AR2 | C5a receptor 2 | 36,000 | C5a | – | 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
editDeficits 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
editReferences
edit- ^ a b c d e 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.
- ^ Verschoor A, Kemper C, Köhl J (15 September 2017). "Complement Receptors". eLS: 1–17. doi:10.1002/9780470015902.a0000512.pub3. ISBN 9780470015902.
- ^ Carroll MC (December 2008). "Complement and humoral immunity". Vaccine. 26 (Suppl 8): I28-33. doi:10.1016/j.vaccine.2008.11.022. PMC 4018718. PMID 19388161.
- ^ a b c 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.
- ^ Parham P (2005). The Immune System (2nd ed.). Garland Science. ISBN 9780815340935.
- ^ Schwartz RA, Thomas I. "Complement Receptor Deficiency: eMedicine Dermatology". Medscape. Retrieved 7 December 2010.
External links
edit- Complement receptors at the U.S. National Library of Medicine Medical Subject Headings (MeSH)