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{{Multiple issues| {{expert-subject|date=September 2008}} {{refimprove|date=September 2008}}}}
{{Use dmy dates|date=July 2013}}
{{Pfam_box
| Symbol = Complement receptor
| Name = Complement receptor
| image =
| width =
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| InterPro=
| SMART=
| PROSITE =
| SCOP =
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| OPM family=
| OPM protein=
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| Membranome family= 116
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A '''complement receptor''' is a membrane-bound [[receptor (biochemistry)|receptor]] belonging to the [[complement system]], which is part of the [[innate immune system]]. Complement receptors bind [[Effector (biology)|effector]] [[protein]] fragments that are produced in response to antigen-antibody complexes or damage-associated molecules.<ref name="ar14">{{cite journal | vauthors = Holers VM | title = Complement and its receptors: new insights into human disease | journal = Annual Review of Immunology | volume = 32 | pages = 433–59 | date = 29 January 2014 | pmid = 24499275 | doi = 10.1146/annurev-immunol-032713-120154 }}</ref> Complement receptor activation contributes to the regulation of [[inflammation]], [[leukocyte extravasation]], and [[phagocytosis]]; it also contributes to the [[adaptive immune system|adaptive immune response]].<ref name="cr17">{{cite journal|title=Complement Receptors |vauthors=Verschoor A, Kemper C, Köhl J |journal=eLS |date = 15 September 2017 |pages=1–17 |doi=10.1002/9780470015902.a0000512.pub3 |isbn=9780470015902 }}</ref><ref name="pmid19388161">{{cite journal | vauthors = Carroll MC | title = Complement and humoral immunity | journal = Vaccine | volume = 26 Suppl 8 | issue = Suppl 8 | pages = I28-33 | date = December 2008 | pmid = 19388161 | pmc = 4018718 | doi = 10.1016/j.vaccine.2008.11.022 }}</ref> Different complement receptors can participate in either the [[classical complement pathway]], the [[alternative complement pathway]], or both.<ref name="Janeway 2001">{{cite book|url=https://www.ncbi.nlm.nih.gov/books/NBK27100|chapter=The complement system and innate immunity| vauthors = Janeway Jr CA, Travers P, Walport M, Shlomchik MJ |year=2001|edition=5th|title=Immunobiology: The Immune System in Health and Disease|publisher=Garland Science|access-date=2020-06-17|location=New York }}</ref>

== Expression and function ==
[[White blood cell]]s, particularly [[monocyte]]s and [[macrophage]]s, [[gene expression|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.<ref name="ar14"/> Complement receptor (CR) 1, 3, and 4 function as [[opsonin]]s which stimulate [[phagocytosis]], whereas CR2 is expressed only on [[B cell]]s as a [[co-receptor]].

[[Red blood cell]]s (RBCs) also express CR1, which enables RBCs to carry complement-bound [[antigen-antibody complex]]es to the [[liver]] and [[spleen]] for degradation.<ref>{{cite book | first = Peter | last = Parham | name-list-format = vanc |title=The Immune System |edition=2nd|publisher=Garland Science|isbn=9780815340935}}</ref>

{| class="wikitable"
! CR # || Name || Molecular weight (Da, approx.)<ref name="ar14"/> || [[Ligand (biochemistry)|Ligand]]<ref name="Janeway 2001" /> || [[Cluster of differentiation|CD]] || Major cell types<ref name="Janeway 2001"/>{{ref|A|a}} || Major activities<ref name="ar14"/>
|-
| 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 α<sub>M</sub>β<sub>2</sub>" || 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.{{note|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 | Complement system#Role in disease | Classical complement pathway#Clinical significance | Alternative complement pathway#Role in disease}}
Deficits in complement receptor expression can cause disease.<ref name="eMedicine Dermatology">{{cite web | vauthors = Schwartz RA, Thomas I |url=http://emedicine.medscape.com/article/1051238-overview |title=Complement Receptor Deficiency: eMedicine Dermatology |website=Medscape |access-date=2010-12-07}}</ref> Mutations in complement receptors which alter receptor function can also increase risk of certain diseases.<ref name="ar14"/>

== See also ==
* [[Complement system]]
* [[Humoral immunity]]
* [[Immune system]]

== References ==
{{Reflist}}

== External links ==
* {{MeshName|Complement+receptors}}

{{Complement system}}
{{Pattern recognition receptors}}

[[Category:Complement system]]
[[Category:Single-pass transmembrane proteins]]
{{dictionary-stub1}}

Complement receptor - Revision history

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Prab at 16:51, 22 March 2025

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