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FCER1

From Wikipedia, the free encyclopedia
(Redirected fromFcεRI)
The structure of the FcεRI receptor
Summary of IgE/FcεRI receptor mediated downward signal cascade
High-affinity IgE receptor; Alpha
Identifiers
SymbolFCER1A
Alt. symbolsFcεRIα, FCE1A
NCBI gene2205
HGNC3609
OMIM147140
RefSeqNM_002001
UniProtP12319
Other data
LocusChr. 1q23
Search for
StructuresSwiss-model
DomainsInterPro
High affinity IgE receptor; beta
Identifiers
SymbolMS4A2
Alt. symbolsFcεRIβ, FCER1B, IGER, APY
NCBI gene2206
HGNC7316
OMIM147138
RefSeqNM_000139
UniProtQ01362
Other data
LocusChr. 1q23
Search for
StructuresSwiss-model
DomainsInterPro
High affinity IgE receptor; gamma
Identifiers
SymbolFCER1G
Alt. symbolsFcεRIγ
NCBI gene2207
HGNC3611
OMIM147139
RefSeqNM_004106
UniProtP30273
Other data
LocusChr. 1q23
Search for
StructuresSwiss-model
DomainsInterPro

Thehigh-affinity IgE receptor,also known asFcεRI,orFc epsilon RI,is the high-affinityreceptorfor theFc regionofimmunoglobulin E(IgE), anantibodyisotypeinvolved inallergydisorders andparasiteimmunity. FcεRI is atetramericreceptor complex that binds Fc portion of the εheavy chainofIgE.[1]It consists of one Alpha (FcεRIα– antibody binding site), one beta (FcεRIβ– which amplifies the downstream signal), and two gamma chains (FcεRIγ– the site where the downstream signal initiates) connected by two disulfide bridges onmast cellsandbasophils.It lacks the beta subunit on other cells. It is constitutively expressed on mast cells and basophils[2]and is inducible ineosinophils.

Tissue distribution

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FcεRI is found on epidermalLangerhans cells,eosinophils, mast cells, and basophils.[3][4][5]As a result of its cellular distribution, this receptor plays a major role in controllingallergic responses.FcεRI is also expressed onantigen-presenting cells,and controls the production of important immune mediators (cytokines,interleukins,leukotrienes,andprostaglandins) that promoteinflammation.[6]The most known mediator ishistamine,which results in the five symptoms of inflammation: heat, swelling, pain, redness and loss of function.

FcεRI was demonstrated in bronchial/tracheal airwaysmooth muscle cellsin normal and asthmatic patients. FcεRI cross-linking by IgE and anti-IgE antibodies led to Th2 (IL-4, -5, and -13) cytokines and CCL11/eotaxin-1 chemokine release; and ([Ca2+]i) mobilization, suggesting a likely IgE-FcεRI-ASM (airwaysmooth muscle cell)-mediated link to airway inflammation andairway hyperresponsiveness.[7][8]

Mechanism of action

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Crosslinking of the FcεRI via IgE-antigencomplexes leads to degranulation of mast cells or basophils and release ofinflammatorymediators.[9]Under laboratory conditions,degranulationof isolated basophils can also be induced withantibodiesto the FcεRIα, which crosslink the receptor. Such crosslinking and potentially pathogenicautoantibodiesto the FcεRIα have been isolated from humancord blood,which suggest that they occur naturally and are present already at birth. However, theirepitopeon FcεRIα was masked by IgE, and the affinity of the corresponding autoantibodies found in healthy adults appeared lowered.[10]

See also

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References

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  1. ^Kumar, Vinay; Abbas, Abul K.; Aster, Jon (2012-05-01).Robbins Basic Pathology(9 ed.). Saunders.
  2. ^Pawankar R (February 2001). "Mast cells as orchestrators of the allergic reaction: the IgE-IgE receptor mast cell network".Current Opinion in Allergy and Clinical Immunology.1(1): 3–6.doi:10.1097/00130832-200102000-00002.PMID11964662.
  3. ^Ochiai K, Wang B, Rieger A, Kilgus O, Maurer D, Födinger D, Kinet J, Stingl G, Tomioka H (1994). "A review on Fc epsilon RI on human epidermal Langerhans cells".International Archives of Allergy and Immunology.104. Suppl 1 (1): 63–64.doi:10.1159/000236756.PMID8156009.
  4. ^Prussin C, Metcalfe D (1994). "5".Nature.367(6459): 183–6.doi:10.1038/367183a0.PMID8114916.S2CID4331405.
  5. ^Gounni, A.; Lamkhioued, B.; Ochiai, K.; Tanaka, Y.; Delaporte, E.; Capron, A.; Kinet, J.P.; Capron, M. (2006). "IgE, mast cells, basophils, and eosinophils".Journal of Allergy and Clinical Immunology.117(2 Suppl Mini–Primer): S450–5456.doi:10.1016/j.jaci.2005.11.016.PMID16455345.
  6. ^von Bubnoff D, Novak N, Kraft S, Bieber T (2003). "The central role of FcepsilonRI in allergy".Clinical and Experimental Dermatology.28(2): 184–187.doi:10.1046/j.1365-2230.2003.01209.x.PMID12653710.S2CID2080598.
  7. ^Gounni, A.S.; Wellemans, V.; Yang, J.; Bellesort, F.; Kassiri, K.; Gangloff, S.; Guenounou, M.;Halayko, A.J.;Hamid, Q.; Lamkhioued, B. (August 15, 2005)."Human airway smooth muscle cells express the high affinity receptor for IgE (Fc epsilon RI): a critical role of Fc epsilon RI in human airway smooth muscle cell function".Journal of Immunology.175(4): 2613–2621.doi:10.4049/jimmunol.175.4.2613.PMID16081836.
  8. ^Gounni, A.S. (September 2006)."The high-affinity IgE receptor (FcepsilonRI): a critical regulator of airway smooth muscle cells?".American Journal of Physiology.291(3): L312-321.doi:10.1152/ajplung.00005.2006.PMID16581830.
  9. ^Siraganian RP (December 2003)."Mast cell signal transduction from the high-affinity IgE receptor".Current Opinion in Immunology.15(6): 639–646.doi:10.1016/j.coi.2003.09.010.PMID14630197.S2CID39294873.
  10. ^Bobrzynski T, Fux M, Vogel M, Stadler MB, Stadler BM, Miescher SM (November 2005)."A high-affinity natural autoantibody from human cord blood defines a physiologically relevant epitope on the FcepsilonRI Alpha".Journal of Immunology.175(10): 6589–6596.doi:10.4049/jimmunol.175.10.6589.PMID16272313.
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