Complement receptor

From Wikipedia, the free encyclopedia

Complement receptor
Identifiers
SymbolComplement receptor
Membranome116

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]

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 # 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
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. ^ 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.
  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. ^ 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.
  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.

External links[]

Retrieved from ""