408:). Calnexin acts to stabilize the class I MHC α chains prior to β2m binding. Following complete assembly of the MHC molecule, calnexin dissociates. The MHC molecule lacking a bound peptide is inherently unstable and requires the binding of the chaperones calreticulin and Erp57. Additionally, tapasin binds to the MHC molecule and serves to link it to the TAP proteins and facilitates the selection of peptide in an iterative process called peptide editing, thus facilitating enhanced peptide loading and colocalization.
477:(NK) cells are normally inactivated upon recognizing MHC I molecules on the surface of cells. Therefore, in the absence of MHC I molecules, NK cells are activated and recognize the cell as aberrant, suggesting that it may be infected by viruses attempting to evade immune destruction. Several human cancers also show down-regulation of MHC I, giving transformed cells the same survival advantage of being able to avoid normal immune surveillance designed to destroy any infected or transformed cells.
322:
462:. As viruses induce cellular expression of viral proteins, some of these products are tagged for degradation, with the resulting peptide fragments entering the endoplasmic reticulum and binding to MHC I molecules. It is in this way, the MHC class I-dependent pathway of antigen presentation, that the virus infected cells signal T-cells that abnormal proteins are being produced as a result of infection.
42:
341:
activity. The proteasome degrades intracellular proteins into small peptides that are then released into the cytosol. Proteasomes can also ligate distinct peptide fragments (termed spliced peptides), producing sequences that are noncontiguous and therefore not linearly templated in the genome. The
175:
A normal cell will display peptides from normal cellular protein turnover on its class I MHC, and CTLs will not be activated in response to them due to central and peripheral tolerance mechanisms. When a cell expresses foreign proteins, such as after viral infection, a fraction of the class I MHC
638:(death) of one copy of the gene, though sometimes this process results in two new genes with divergent function. It is likely that human MHC class Ib loci (HLA-E, -F, and -G) as well as MHC class I pseudogenes arose from MHC class Ia loci (HLA-A, -B, and -C) in this birth-and-death process.
473:, reducing the risk of infecting neighboring cells. As an evolutionary response to this method of immune surveillance, many viruses are able to down-regulate or otherwise prevent the presentation of MHC class I molecules on the cell surface. In contrast to cytotoxic T lymphocytes,
164:. The MHC I: peptide complex is then inserted via the endoplasmic reticulum into the external plasma membrane of the cell. The epitope peptide is bound on extracellular parts of the class I MHC molecule. Thus, the function of the class I MHC is to display intracellular proteins to
1721:
297:
domains fold to make up a groove for peptides to bind. MHC class I molecules bind peptides that are predominantly 8-10 amino acid in length (Parham 87), but the binding of longer peptides have also been reported.
598:, and have been found in all living jawed vertebrates that have been studied thus far. Since their emergence in jawed vertebrates, this gene family has been subjected to many divergent evolutionary paths as
1418:
Albring J, Koopmann JO, Hämmerling GJ, Momburg F (January 2004). "Retrotranslocation of MHC class I heavy chain from the endoplasmic reticulum to the cytosol is dependent on ATP supply to the ER lumen".
706:
Kulski JK, Shiina T, Anzai T, Kohara S, Inoko H (December 2002). "Comparative genomic analysis of the MHC: the evolution of class I duplication blocks, diversity and complexity from shark to man".
325:
Simplified diagram of cytoplasmic protein degradation by the proteasome, transport into endoplasmic reticulum by TAP complex, loading on MHC class I, and transport to the surface for presentation
113:; this will trigger an immediate response from the immune system against a particular non-self antigen displayed with the help of an MHC class I protein. Because MHC class I molecules present
1714:
342:
origin of spliced peptide segments can be from the same protein (cis-splicing) or different proteins (trans-splicing). The peptides have to be translocated from the cytosol into the
751:
1707:
1285:
Wearsch PA, Cresswell P (August 2007). "Selective loading of high-affinity peptides onto major histocompatibility complex class I molecules by the tapasin-ERp57 heterodimer".
1063:
Faridi P, Li C, Ramarathinam SH, Vivian JP, Illing PT, Mifsud NA, Ayala R, Song J, Gearing LJ, Hertzog PJ, Ternette N, Rossjohn J, Croft NP, Purcell AW (12 October 2018).
183:(NKs). Reduction in the normal levels of surface class I MHC, a mechanism employed by some viruses and certain tumors to evade CTL responses, activates NK cell killing.
377:. The two subunits form a peptide binding site and two ATP binding sites that face the cytosol. TAP binds peptides on the cytoplasmic side and translocates them under
439:
channel into the cytosol, where they might undergo further trimming in size, and might be translocated by TAP back into ER for binding to a MHC class I molecule.
362:
2102:
1175:
Blees A, Januliene D, Hofmann T, Koller N, Schmidt C, Trowitzsch S, Moeller A, Tampé R (November 2017). "Structure of the human MHC-I peptide-loading complex".
2605:
1497:"Activation of CXCR4 triggers ubiquitination and down-regulation of major histocompatibility complex class I (MHC-I) on epithelioid carcinoma HeLa cells"
634:
events cause the genome to contain multiple copies of a gene which can then undergo separate evolutionary processes. Sometimes these processes result in
2155:
176:
will display these peptides on the cell surface. Consequently, CTLs specific for the MHC:peptide complex will recognize and kill presenting cells.
2243:
1538:"Trans-species polymorphism in humans and the great apes is generally maintained by balancing selection that modulates the host immune response"
2334:
1064:
1456:"Exogenous antigens are processed through the endoplasmic reticulum-associated degradation (ERAD) in cross-presentation by dendritic cells"
1379:"Export of antigenic peptides from the endoplasmic reticulum intersects with retrograde protein translocation through the Sec61p channel"
904:
Ljunggren HG, Stam NJ, Öhlén C, Neefjes JJ, Höglund P, Heemels MT, Bastin J, Schumacher TN, Townsend A, Kärre K, Ploegh HL (1990-08-02).
748:
1847:
2534:
2343:
1992:
82:
435:
Peptides that fail to bind MHC class I molecules in the lumen of the endoplasmic reticulum (ER) are removed from the ER via the
998:
Sun Y, Young MC, Woodward CH, Danon JN, Truong HV, Gupta S, Winters TJ, Font-Burgada J, Burslem GM, Sgourakis NG (2023-06-20).
381:
consumption into the lumen of the ER. The MHC class I molecule is then, in turn, loaded with peptides in the lumen of the ER.
416:
818:
Syken J, Grandpre T, Kanold PO, Shatz CJ (September 2006). "PirB restricts ocular-dominance plasticity in visual cortex".
1699:
1107:
Liepe J, Marino F, Sidney J, Jeko A, Bunting DE, Sette A, Kloetzel PM, Stumpf MP, Heck AJ, Mishto M (21 October 2016).
2144:
415:
to reach the cell surface. The transport of the MHC class I molecules through the secretory pathway involves several
2600:
2564:
2327:
1734:
411:
Once the peptide is loaded onto the MHC class I molecule, the complex dissociates and it leaves the ER through the
2554:
1377:
Koopmann JO, Albring J, Hüter E, Bulbuc N, Spee P, Neefjes J, Hämmerling GJ, Momburg F, et al. (July 2000).
1330:"Tapasin shapes immunodominance hierarchies according to the kinetic stability of peptide-MHC class I complexes"
869:
Burrows SR, Rossjohn J, McCluskey J (January 2006). "Have we cut ourselves too short in mapping CTL epitopes?".
191:
Paired-immunoglobulin-like receptor B (PirB), an MHCI-binding receptor, is involved in the regulation of visual
168:(CTLs). However, class I MHC can also present peptides generated from exogenous proteins, in a process known as
1693:
1683:
1679:
1108:
1065:"A subset of HLA-I peptides are not genomically templated: Evidence for cis- and trans-spliced peptide ligands"
1000:"Universal open MHC-I molecules for rapid peptide loading and enhanced complex stability across HLA allotypes"
768:
Hansen TH, Bouvier M (July 2009). "MHC class I antigen presentation: learning from viral evasion strategies".
619:
305:
between the peptide, MHC I, and B2M, under subphysiological temperatures, stable, peptide-deficient MHC I/B2M
384:
The peptide-loading process involves several other molecules that form a large multimeric complex called the
2529:
385:
254:
133:
610:
in an evolutionary related MHC class I gene remains in two species, likely due to strong pathogen-mediated
419:
of the MHC molecule. Some of the posttranslational modifications occur in the ER and involve change to the
2595:
2590:
2559:
591:
470:
378:
196:
2320:
1908:
1730:
603:
343:
749:
http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/H/HLA.html#Class_I_Histocompatibility_Molecules
1808:
1239:
1184:
1123:
1011:
917:
827:
258:
242:
180:
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have been observed. Synthetic stable, peptide-receptive MHC I molecules have been generated using a
611:
226:
65:
1359:
1310:
1208:
1157:
851:
793:
731:
169:
2107:
960:
1328:
Thirdborough SM, Roddick JS, Radcliffe JN, Howarth M, Stevenson FK, Elliott T (February 2008).
2539:
2188:
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2115:
1659:
1618:
1569:
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1027:
980:
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933:
886:
843:
785:
723:
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622:
evolution is one of the mechanistic explanations for the size of the MHC class I gene family.
595:
575:
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555:
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412:
217:
became more pronounced at all ages. PirB loss of function mutant mice also exhibited enhanced
110:
2233:
2213:
2203:
2198:
2168:
1689:
301:
While a high-affinity peptide and the B2M subunit are normally required to maintain a stable
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211:
200:
165:
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1604:
361:
The peptide translocation from the cytosol into the lumen of the ER is accomplished by the
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2020:
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1537:
961:"Direct binding of peptide to empty MHC class I molecules on intact cells and in vitro"
680:
655:
474:
455:
351:
337:. The proteasome is a macromolecule that consists of 28 subunits, of which half affect
321:
310:
106:
1395:
1378:
1262:
1227:
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976:
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671:
241:
MHC class I molecules are heterodimers that consist of two polypeptide chains, α and
230:
109:. Their function is to display peptide fragments of proteins from within the cell to
1363:
1314:
1161:
735:
2395:
2002:
1212:
1109:"A large fraction of HLA class I ligands are proteasome-generated spliced peptides"
959:
Schumacher TN, Heemels MT, Neefjes JJ, Kast W, Melief CJ, Ploegh HL (August 1990).
855:
797:
656:"The MHC class I antigen presentation pathway: strategies for viral immune evasion"
393:
306:
90:
86:
1831:
1228:"Tapasin enhances MHC class I peptide presentation according to peptide half-life"
1432:
454:
MHC class I molecules are loaded with peptides generated from the degradation of
70:
2549:
2049:
1893:
1818:
1785:
1756:
1747:
459:
338:
1232:
Proceedings of the
National Academy of Sciences of the United States of America
1084:
602:
events have taken place. There are, however, documented cases of trans-species
369:
family and is a heterodimeric multimembrane-spanning polypeptide consisting of
249:(B2M). The two chains are linked noncovalently via interaction of B2M and the α
1554:
635:
599:
423:
regions of the protein, followed by extensive changes to the N-glycans in the
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161:
98:
1031:
937:
882:
2061:
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1135:
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346:(ER) to meet the MHC class I molecule, whose peptide-binding site is in the
94:
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heterodimer ligand, and checks the coupled peptide for antigenicity. The α
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102:
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210:
and adulthood. When the function of PirB was abolished in mutant mice,
179:
Alternatively, class I MHC itself can serve as an inhibitory ligand for
41:
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2413:
2408:
2228:
2223:
2218:
2208:
2193:
2178:
2173:
2163:
443:
389:
330:
225:. These results suggest that PirB may be involved in the modulation of
157:
118:
114:
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2301:
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1984:
1975:
1868:
929:
607:
270:
17:
1495:
Wang Z, Zhang L, Qiao A, Watson K, Zhang J, Fan GH (February 2008).
781:
1298:
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generated mainly from the degradation of cytosolic proteins by the
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1956:
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The fate of the virus-infected cell is almost always induction of
436:
405:
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320:
145:
141:
137:
121:
proteins, the pathway of MHC class I presentation is often called
1454:
Imai J, Hasegawa H, Maruya M, Koyasu S, Yahara I (January 2005).
427:. The N-glycans mature fully before they reach the cell surface.
2097:
2092:
2039:
2034:
2024:
1960:
1932:
1916:
1912:
1826:
1803:
1798:
1770:
374:
370:
2316:
1703:
1589:"Concerted and birth-and-death evolution of multigene families"
2071:
2057:
266:
257:, while the B2M subunit is not polymorphic and encoded by the
1226:
Howarth M, Williams A, Tolstrup AB, Elliott T (August 2004).
277:-CD8 interaction holds the MHC I molecule in place while the
1536:
Azevedo L, Serrano C, Amorim A, Cooper DN (September 2015).
265:
domain is plasma membrane-spanning and interacts with the
253:
domain. Only the α chain is polymorphic and encoded by a
281:(TCR) on the surface of the cytotoxic T cell binds its α
758:
Kimball's
Biology Pages, Histocompatibility Molecules
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2013:
1983:
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1867:
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1840:
1817:
1784:
1755:
1744:
64:
56:
51:
34:
906:"Empty MHC class I molecules come out in the cold"
1638:"Origin and evolution of HLA class I pseudogenes"
442:For example, an interaction of sec61 with bovine
1004:Proceedings of the National Academy of Sciences
313:between the MHC I and B2M, named "open MHC-I".
363:transporter associated with antigen processing
2328:
1715:
590:The MHC class I genes originated in the most
8:
813:
811:
809:
807:
2335:
2321:
2313:
1980:
1898:
1873:
1864:
1752:
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1708:
1700:
40:
1692:at the U.S. National Library of Medicine
1682:at the U.S. National Library of Medicine
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1612:
1563:
1553:
1512:
1471:
1394:
1345:
1261:
1251:
1143:
1083:
1039:
679:
606:in MHC class I genes, where a particular
329:The peptides are generated mainly in the
646:
630:Birth-and-death evolution asserts that
350:of the ER. They have membrane proximal
221:after monocular deprivation during the
46:Schematic representation of MHC class I
1605:10.1146/annurev.genet.39.073003.112240
31:
1655:10.1093/oxfordjournals.molbev.a040201
7:
701:
699:
626:Birth-and-death of MHC class I genes
1680:Histocompatibility+Antigens+Class+I
1501:The Journal of Biological Chemistry
2606:Single-pass transmembrane proteins
81:are one of two primary classes of
25:
1848:Polymeric immunoglobulin receptor
357:Translocation and peptide loading
136:corresponding to MHC class I are
85:(MHC) molecules (the other being
2535:Minor histocompatibility antigen
2344:Major histocompatibility complex
720:10.1034/j.1600-065x.2002.19008.x
672:10.1046/j.1365-2567.2003.01738.x
83:major histocompatibility complex
1642:Molecular Biology and Evolution
1587:Nei M, Rooney AP (2005-11-14).
417:posttranslational modifications
2060:(with two glycoprotein chains
1334:European Journal of Immunology
618:that can infect both species.
365:(TAP). TAP is a member of the
1:
2156:Killer-cell IG-like receptors
1396:10.1016/S1074-7613(00)00013-3
1433:10.1016/j.molimm.2003.08.008
977:10.1016/0092-8674(90)90020-F
27:Protein of the immune system
2244:Leukocyte IG-like receptors
195:. PirB is expressed in the
156:Class I MHC molecules bind
2622:
2565:Cluster of differentiation
1735:immunoglobulin superfamily
1085:10.1126/sciimmunol.aar3947
770:Nature Reviews. Immunology
654:Hewitt EW (October 2003).
187:PirB and visual plasticity
2555:Human blood group systems
1593:Annual Review of Genetics
1555:10.1186/s40246-015-0043-1
39:
1694:Medical Subject Headings
1684:Medical Subject Headings
1636:Hughes AL (March 1995).
1460:International Immunology
883:10.1016/j.it.2005.11.001
2560:Cell adhesion molecules
2530:Human leukocyte antigen
1731:Transmembrane receptors
1253:10.1073/pnas.0306294101
1136:10.1126/science.aaf4384
1024:10.1073/pnas.2304055120
840:10.1126/science.1128232
386:Peptide loading complex
97:cells in the bodies of
89:) and are found on the
1514:10.1074/jbc.m706848200
592:recent common ancestor
471:cell-mediated immunity
458:cytosolic proteins in
326:
197:central nervous system
1473:10.1093/intimm/dxh184
1347:10.1002/eji.200737832
708:Immunological Reviews
344:endoplasmic reticulum
324:
206:in the developmental
101:. They also occur on
79:MHC class I molecules
1421:Molecular Immunology
871:Trends in Immunology
586:Evolutionary history
259:Beta-2 microglobulin
181:natural killer cells
2081:Accessory molecules
1946:Accessory molecules
1244:2004PNAS..10111737H
1197:10.1038/nature24627
1189:2017Natur.551..525B
1128:2016Sci...354..354L
1016:2023PNAS..12004055S
1010:(25): e2304055120.
922:1990Natur.346..476L
832:2006Sci...313.1795S
612:balancing selection
446:has been observed.
388:consisting of TAP,
227:synaptic plasticity
2145:cytokine receptors
1745:Antibody receptor:
1072:Science Immunology
826:(5794): 1795–800.
754:2016-02-04 at the
481:Genes and isotypes
327:
170:cross-presentation
127:endogenous pathway
2601:Protein targeting
2573:
2572:
2540:Blood transfusion
2310:
2309:
2135:Cytokine receptor
2129:
2128:
2125:
2124:
1970:
1969:
1941:
1940:
1856:
1855:
1690:MHC+Class+I+Genes
1287:Nature Immunology
1183:(7681): 525–528.
1122:(6310): 354–358.
916:(6283): 476–480.
596:jawed vertebrates
527:Less polymorphic
486:Very polymorphic
450:Effect of viruses
413:secretory pathway
166:cytotoxic T cells
111:cytotoxic T cells
76:
75:
16:(Redirected from
2613:
2337:
2330:
2323:
2314:
2014:Antigen receptor
1981:
1899:
1877:Antigen receptor
1874:
1865:
1861:Antigen receptor
1819:Alpha (α)/mu (μ)
1753:
1738:immune receptors
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1238:(32): 11737–42.
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1078:(28): eaar3947.
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636:pseudogenization
632:gene duplication
212:ocular dominance
201:ocular dominance
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782:10.1038/nri2575
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756:Wayback Machine
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620:Birth-and-death
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431:Peptide removal
425:Golgi apparatus
367:ABC transporter
359:
319:
303:ternary complex
296:
292:
288:
284:
279:T cell receptor
276:
269:co-receptor of
264:
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223:critical period
208:critical period
199:and diminishes
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132:In humans, the
107:red blood cells
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1674:External links
1672:
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1628:
1579:
1542:Human Genomics
1528:
1487:
1446:
1427:(10): 733–41.
1410:
1369:
1320:
1299:10.1038/ni1485
1277:
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1167:
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971:(3): 563–567.
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1599:(1): 121–52.
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776:(7): 503–13.
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623:
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617:
613:
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604:polymorphisms
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546:
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456:ubiquitinated
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236:
234:
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231:visual cortex
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139:
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128:
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120:
117:derived from
116:
112:
108:
105:, but not on
104:
100:
96:
92:
88:
84:
80:
72:
69:
67:
63:
59:
55:
50:
43:
38:
33:
30:
19:
2396:MHC class II
2352:
2142:
2050:Co-receptors
2003:MHC class II
1997:
1645:
1641:
1631:
1596:
1592:
1582:
1545:
1541:
1531:
1504:
1500:
1490:
1466:(1): 45–53.
1463:
1459:
1449:
1424:
1420:
1413:
1386:
1382:
1372:
1340:(2): 364–9.
1337:
1333:
1323:
1290:
1286:
1280:
1235:
1231:
1221:
1180:
1176:
1170:
1119:
1115:
1102:
1075:
1071:
1058:
1007:
1003:
993:
968:
964:
954:
913:
909:
899:
874:
870:
864:
823:
819:
773:
769:
763:
744:
711:
707:
666:(2): 163–9.
663:
659:
649:
629:
589:
579:(pseudogene)
574:
571:(pseudogene)
566:
554:
542:
530:
513:
501:
489:
464:
453:
441:
434:
410:
394:calreticulin
383:
360:
328:
307:heterodimers
300:
240:
190:
178:
174:
155:
131:
126:
122:
91:cell surface
87:MHC class II
78:
77:
29:
2550:Calgranulin
2353:MHC class I
1998:MHC class I
1894:Co-receptor
1757:Epsilon (ε)
1748:Fc receptor
877:(1): 11–6.
460:proteasomes
339:proteolytic
261:gene. The α
99:vertebrates
60:MHC class I
52:Identifiers
35:MHC class I
2580:Categories
1902:stimulate:
714:: 95–122.
660:Immunology
642:References
600:speciation
335:proteasome
219:plasticity
215:plasticity
204:plasticity
193:plasticity
162:proteasome
66:Membranome
1841:Secretory
1786:Gamma (γ)
1548:(1): 21.
1032:0027-8424
938:0028-0836
616:pathogens
467:apoptosis
317:Synthesis
237:Structure
123:cytosolic
119:cytosolic
103:platelets
95:nucleated
2545:Arrestin
2189:KIR2DL5B
2184:KIR2DL5A
1926:inhibit:
1809:Neonatal
1623:16285855
1574:26337052
1523:18083706
1482:15546887
1441:14644099
1405:10933400
1383:Immunity
1364:28659293
1356:18196518
1315:29762957
1307:17603487
1272:15286279
1205:29107940
1162:41095551
1154:27846572
1094:30315122
1050:37310998
1041:10288639
891:16297661
848:16917027
790:19498380
752:Archived
736:41765680
728:12493009
690:14511229
469:through
421:N-glycan
398:calnexin
255:HLA gene
158:peptides
152:Function
115:peptides
2346:classes
2234:KIR3DS1
2229:KIR3DL3
2224:KIR3DL2
2219:KIR3DL1
2214:KIR2DS5
2209:KIR2DS4
2204:KIR2DS3
2199:KIR2DS2
2194:KIR2DS1
2179:KIR2DL4
2174:KIR2DL3
2169:KIR2DL2
2164:KIR2DL1
2108:ζ-chain
1985:Ligands
1976:T cells
1869:B cells
1804:FcγRIII
1664:7700152
1614:1464479
1565:4559023
1240:Bibcode
1213:4447406
1185:Bibcode
1124:Bibcode
1116:Science
1012:Bibcode
985:2199065
946:2198471
918:Bibcode
856:1860730
828:Bibcode
820:Science
798:9278263
681:1783040
594:of all
444:albumin
390:tapasin
352:Ig fold
333:by the
331:cytosol
273:. The α
271:T-cells
229:in the
93:of all
2487:HLA-DR
2455:HLA-DQ
2438:HLA-DP
2421:HLA-DO
2404:HLA-DM
2302:LILRB5
2297:LILRB4
2292:LILRB3
2287:LILRB2
2282:LILRB1
2277:LILRA6
2272:LILRA5
2267:LILRA4
2262:LILRA3
2257:LILRA2
2252:LILRA1
1832:Fcα/μR
1799:FcγRII
1771:FcεRII
1696:(MeSH)
1686:(MeSH)
1662:
1621:
1611:
1572:
1562:
1521:
1480:
1439:
1403:
1362:
1354:
1313:
1305:
1270:
1263:511045
1260:
1211:
1203:
1177:Nature
1160:
1152:
1092:
1048:
1038:
1030:
983:
944:
936:
910:Nature
889:
854:
846:
796:
788:
734:
726:
688:
678:
608:allele
400:, and
144:, and
57:Symbol
2586:Genes
2523:Other
2386:HLA-G
2381:HLA-F
2376:HLA-E
2371:HLA-C
2366:HLA-B
2361:HLA-A
1827:FcαRI
1794:FcγRI
1765:FcεRI
1360:S2CID
1311:S2CID
1209:S2CID
1158:S2CID
1112:(PDF)
1068:(PDF)
852:S2CID
794:S2CID
732:S2CID
576:HLA-L
568:HLA-K
561:HLA-G
556:HLA-G
549:HLA-F
544:HLA-F
537:HLA-E
532:HLA-E
520:HLA-C
515:HLA-C
508:HLA-B
503:HLA-B
496:HLA-A
491:HLA-A
437:sec61
406:PDIA3
402:Erp57
348:lumen
293:and α
146:HLA-C
142:HLA-B
138:HLA-A
18:MHC I
2143:see
2116:TCRζ
2114:and
2112:CD3ζ
2103:CD3ε
2098:CD3δ
2093:CD3γ
2066:CD8β
2064:and
2062:CD8α
2040:TRG@
2035:TRD@
2030:TRB@
2025:TRA@
1961:CD79
1957:Ig-β
1953:Ig-α
1933:CD22
1917:CD81
1913:CD19
1909:CD21
1660:PMID
1619:PMID
1570:PMID
1519:PMID
1478:PMID
1437:PMID
1401:PMID
1352:PMID
1303:PMID
1268:PMID
1201:PMID
1150:PMID
1090:PMID
1046:PMID
1028:ISSN
981:PMID
965:Cell
942:PMID
934:ISSN
887:PMID
844:PMID
786:PMID
724:PMID
686:PMID
375:TAP2
373:and
371:TAP1
134:HLAs
2088:CD3
2072:CD4
2058:CD8
2021:TCR
1993:MHC
1884:BCR
1773:is
1650:doi
1609:PMC
1601:doi
1560:PMC
1550:doi
1509:doi
1505:283
1468:doi
1429:doi
1391:doi
1342:doi
1295:doi
1258:PMC
1248:doi
1236:101
1193:doi
1181:551
1140:hdl
1132:doi
1120:354
1080:doi
1036:PMC
1020:doi
1008:120
973:doi
926:doi
914:346
879:doi
836:doi
824:313
778:doi
716:doi
712:190
676:PMC
668:doi
664:110
614:by
379:ATP
267:CD8
125:or
2582::
2512:β5
2507:β4
2502:β3
2497:β1
2480:β3
2475:β2
2470:β1
2465:α2
2460:α1
2448:β1
2443:α1
2023::
1733::
1658:.
1646:12
1644:.
1640:.
1617:.
1607:.
1597:39
1595:.
1591:.
1568:.
1558:.
1544:.
1540:.
1517:.
1503:.
1499:.
1476:.
1464:17
1462:.
1458:.
1435:.
1425:40
1423:.
1399:.
1387:13
1385:.
1381:.
1358:.
1350:.
1338:38
1336:.
1332:.
1309:.
1301:.
1289:.
1266:.
1256:.
1246:.
1234:.
1230:.
1207:.
1199:.
1191:.
1179:.
1156:.
1148:.
1138:.
1130:.
1118:.
1114:.
1088:.
1074:.
1070:.
1044:.
1034:.
1026:.
1018:.
1006:.
1002:.
979:.
969:62
967:.
963:.
940:.
932:.
924:.
912:.
908:.
885:.
875:27
873:.
850:.
842:.
834:.
822:.
806:^
792:.
784:.
772:.
730:.
722:.
710:.
698:^
684:.
674:.
662:.
658:.
396:,
392:,
285:-α
233:.
172:.
148:.
140:,
129:.
71:63
2492:α
2431:β
2426:α
2414:β
2409:α
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