658:
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29:
256:). The peptide presented regulates how T cells respond to an infection. Stable peptide binding is essential to prevent detachment and degradation of a peptide, which could occur without secure attachment to the MHC molecule. This would prevent T cell recognition of the antigen, T cell recruitment, and a proper immune response. The triggered appropriate immune response may include localized
373:, while other cells such as dendritic cells internalize antigens via receptor-mediated endocytosis and create MHC class II molecules plus peptide in the endosomal-lysosomal antigen processing compartment which is independent of the synthesis of new MHC class II complexes. These suggest that after the antigen is internalized, already existent MHC class II complexes on mature
691:
interact and activate the B cells. Normally when B cells are activated they divide, proliferate and differentiate, which includes the differentiation of these cells into plasma cells which are responsible for producing antibodies. However, when there is a deficiency in MHC class II molecules B cells are not activated and cannot differentiate into
200:
of the chains come together to make a membrane-distal peptide-binding domain, while the α2 and β2 regions, the remaining extracellular parts of the chains, form a membrane-proximal immunoglobulin-like domain. The antigen binding groove, where the antigen or peptide binds, is made up of two α-helixes walls and β-sheet.
247:
Having MHC class II molecules present proper peptides that are bound stably is essential for overall immune function. Because class II MHC is loaded with extracellular proteins, it is mainly concerned with presentation of extracellular pathogens (for example, bacteria that might be infecting a wound
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Unlike MHC I, MHC II is meant to present extracellular pathogens rather than intracellular. Furthermore, the first step is to acquire the pathogen through phagocytosis. The pathogen is then broken down in a lysosome and a desired component is then acquired and loaded onto a MHC II molecule. The MHC
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gene; each domain is usually encoded by a different exon within the gene, and some genes have further domains that encode leader sequences, transmembrane sequences, etc. These molecules have both extracellular regions as well as a transmembrane sequence and a cytoplasmic tail. The α1 and β1 regions
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which normally participate in the immune response. Not only do the deficient MHC class II molecules affect the activation and proliferation of T cells but also the rest of the immune response cascade which includes B cells. Therefore, with this decrease in the number of T cells, the T cells cannot
228:, which is the MHC class II transactivator. CIITA is solely expressed on professional APCs; however, non-professional APCs can also regulate CIITA activity and MHC II expression. As mentioned interferon γ (IFN γ) triggers the expression of CIITA and is also responsible for converting
334:. The nascent MHC class II protein in the rough ER has its peptide-binding cleft blocked by the invariant chain (Ii; a trimer) to prevent it from binding cellular peptides or peptides from the endogenous pathway (such as those that would be loaded onto class I MHC).
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Because the antigen-binding groove of MHC class II molecules is open at both ends while the corresponding groove on class I molecules is closed at each end, the antigens presented by MHC class II molecules are longer, generally between 15 and 24
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which are unable to perform as they are expected. The only current form of treatment is a bone-marrow transplant however even this does not cure the disease and most patients do not live past age ten.
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Steimle V, Otten LA, Zufferey M, Mach B (June 2007). "Complementation cloning of an MHC class II transactivator mutated in hereditary MHC class II deficiency (or bare lymphocyte syndrome). 1993".
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195:, but in this case consist of two homogenous peptides, an α and β chain, both of which are encoded in the MHC. The subdesignation α1, α2, etc. refers to separate domains within the
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Paul P, van den Hoorn T, Jongsma ML, Bakker MJ, Hengeveld R, Janssen L, Cresswell P, Egan DA, van Ham M, Ten Brinke A, Ovaa H, Beijersbergen RL, Kuijl C, Neefjes J (April 2011).
390:. MHC II activate helper T cells which help release cytokines and other things which will help induce other cells which help to combat the pathogens outside the cells.
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present. Deficient MHC class II molecules are unable to present antigens to T cells and properly activate T cells. T cells are then unable to proliferate, and secrete
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After MHC class II complexes are synthesized and presented on APCs they are unable to be expressed on the cell surface indefinitely, due to the internalization of the
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674:, is due to mutations in the genes that code for transcription factors that regulate the expression of the MHC class II genes. It results in the depletion of
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341:, followed by fusion with a late endosome containing endocytosed, degraded proteins. The invariant chain is then broken down in stages by proteases called
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During synthesis of class II MHC in the endoplasmic reticulum, the α and β chains are produced and complexed with a special polypeptide known as the
224:. They are expressed on the epithelial cells in the thymus and on APCs in the periphery. MHC class II expression is closely regulated in APCs by
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711:. HLA class II genes are the most important genes associated with the risk of inheriting Type I diabetes, accounting for about 40-50% of
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of these genes that affect peptide binding to the MHC class II molecules seem to impact Type I diabetes risk the most. Specific allele
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by the APCs(antigen presenting cells). In some cells, antigens bind to recycled MHC class II molecules while they are in the early
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have been identified to increase the risk (such as DRB1 and DQB1). Others have been associated with a resistance to the disease.
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removal and allows the binding of peptides with higher affinities. The stable class II MHC is then presented on the cell surface.
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1996:
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Jones EY, Fugger L, Strominger JL, Siebold C (April 2006). "MHC class II proteins and disease: a structural perspective".
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protein that is selectively expressed in immune cells. This protein is localized within MHC-II compartments in immature
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and swelling due to recruitment of phagocytes or may lead to a full-force antibody immune response due to activation of
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Xie Z, Chang C, Zhou Z (October 2014). "Molecular mechanisms in autoimmune type 1 diabetes: a critical review".
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1012:"A Genome-wide multidimensional RNAi screen reveals pathways controlling MHC class II antigen presentation"
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which maintains blockage of the peptide binding cleft on the MHC molecule. A MHC class II-like structure,
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which are MHC class II negative cells into functional APCs that express MHC class II on their surfaces.
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MHC class II genes and molecules are related to a multitude of different diseases, one of which being
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Prigent M, Dubois T, Raposo G, Derrien V, Tenza D, Rossé C, Camonis J, Chavrier P (December 2003).
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1052:"PIK3R2 phosphoinositide-3-kinase, regulatory subunit 2 (beta) [Homo sapiens (human)]"
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Serrano-Martín MM, Moreno-Pérez D, García-Martín FJ, Jurado-Ortiz A (March 2007). "".
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Pathway showing how MHC-II distribution is controlled within
Immature Dendritic Cells.
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PSD4 pleckstrin and Sec7 domain containing 4 [Homo sapiens (human)] - Gene - NCBI
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T cells and some immunoglobulin isotypes even though there are normal levels of both
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The invariant chain also facilitates the export of class II MHC from the ER to the
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866:"The ins and outs of MHC class II-mediated antigen processing and presentation"
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or the blood). Class II molecules interact mainly with immune cells, like the
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is a protein that controls MHC-II compartments with an actin-based mechanism.
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634:(PIP) providing PSD4 with substrates for its GTP loading ability. PSD4 as a
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can be recycled and developed into new MHC class II molecules plus peptide.
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are loaded onto MHC class II molecules prior to their migration to the
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These molecules are constitutively expressed in professional, immune
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II molecule then travels to the surface to present the antigen to a
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In humans, the MHC class II protein complex is encoded by the
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are derived from extracellular proteins (not cytosolic as in
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myofibers. Altogether, this complex contributes to maintain
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Owen JA, Punt J, Stranford SA, Jones PP, Kuby J (2013).
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Pathways controlling MHC class II antigen presentation
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955:"Invariant Chain Structure and MHC Class II Function"
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654:, impeding its translocation to the cell membrane.
179:(BLS), which is a type of MHC class II deficiency.
1230:The immune response basic and clinical principles
670:One type of MHC class II deficiency, also called
607:is an effector of ARL14/ARF7 that interacts with
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924:(7th ed.). New York: W H Freeman & Co.
549:are two kinases that create substrates for PSD4.
538:Several molecules are involved in this pathway.
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175:Mutations in the HLA gene complex can lead to
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118:Loading of a MHC class II molecule occurs by
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826:"Genetic control of MHC class II expression"
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235:MHC class II is also expressed on group 3
146:human leukocyte antigen gene complex (HLA)
96:. These cells are important in initiating
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1354:at the U.S. National Library of Medicine
1344:at the U.S. National Library of Medicine
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318:Learn how and when to remove this message
148:. HLAs corresponding to MHC class II are
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33:Schematic representation of MHC class II
191:molecules, class II molecules are also
72:(MHC) molecules normally found only on
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587:actor) that loads ARL14/ARF7 with GTP.
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695:which causes them to be deficient in
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74:professional antigen-presenting cells
1342:Histocompatibility+Antigens+Class+II
650:loaded vesicles within the immature
300:adding citations to reliable sources
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824:Ting JP, Trowsdale J (April 2002).
381:Antigen processing and presentation
361:Recycling of MHC class II complexes
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1510:Polymeric immunoglobulin receptor
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864:Roche PA, Furuta K (April 2015).
2197:Minor histocompatibility antigen
2006:Major histocompatibility complex
1232:. Amsterdam: Elsevier/Academic.
703:MHC class II and Type I diabetes
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70:major histocompatibility complex
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953:Cresswell, Peter (1996-02-23).
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529:Pathway: PSD4–ARL14/ARF7–MYO1E
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1818:Killer-cell IG-like receptors
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839:10.1016/s0092-8674(02)00696-7
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1228:Mak TW, Saunders ME (2006).
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16:Protein of the immune system
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1906:Leukocyte IG-like receptors
1104:The Journal of Cell Biology
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626:PIK3R2 and PIP5K1A are two
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870:Nature Reviews. Immunology
783:Nature Reviews. Immunology
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832:. 109 Suppl (2): S21-33.
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1356:Medical Subject Headings
1346:Medical Subject Headings
738:Bare lymphocyte syndrome
672:bare lymphocyte syndrome
666:Bare lymphocyte syndrome
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218:antigen-presenting cells
177:bare lymphocyte syndrome
2222:Cell adhesion molecules
2192:Human leukocyte antigen
1393:Transmembrane receptors
636:guanine exchange factor
90:thymic epithelial cells
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642:which binds itself to
107:presented by class II
66:MHC Class II molecules
1203:Journal of Immunology
1116:10.1083/jcb.200305029
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237:innate lymphoid cells
757:"Histocompatibility"
632:Phosphatidylinositol
296:improve this article
130:, and the resulting
1743:Accessory molecules
1608:Accessory molecules
1263:Anales de Pediatria
630:that phosphorylate
1807:cytokine receptors
1407:Antibody receptor:
1352:MHC+Class+II+Genes
733:Cross-presentation
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579:uanine nucleotide
534:Molecules involved
388:helper T cell
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2243:
2228:
2225:
2223:
2220:
2218:
2215:
2213:
2210:
2208:
2205:
2203:
2200:
2198:
2195:
2193:
2190:
2189:
2187:
2183:
2175:
2172:
2170:
2167:
2165:
2162:
2160:
2157:
2155:
2152:
2151:
2150:
2147:
2143:
2140:
2138:
2135:
2133:
2130:
2128:
2125:
2123:
2120:
2119:
2118:
2115:
2111:
2108:
2106:
2103:
2102:
2101:
2098:
2094:
2091:
2089:
2086:
2085:
2084:
2081:
2077:
2074:
2072:
2069:
2068:
2067:
2064:
2063:
2061:
2059:
2055:
2049:
2046:
2044:
2041:
2039:
2036:
2034:
2031:
2029:
2026:
2024:
2021:
2020:
2018:
2016:
2012:
2007:
2000:
1995:
1993:
1988:
1986:
1981:
1980:
1977:
1965:
1962:
1960:
1957:
1955:
1952:
1950:
1947:
1945:
1942:
1940:
1937:
1935:
1932:
1930:
1927:
1925:
1922:
1920:
1917:
1915:
1912:
1911:
1909:
1907:
1903:
1897:
1894:
1892:
1889:
1887:
1884:
1882:
1879:
1877:
1874:
1872:
1869:
1867:
1864:
1862:
1859:
1857:
1854:
1852:
1849:
1847:
1844:
1842:
1839:
1837:
1834:
1832:
1829:
1827:
1824:
1823:
1821:
1819:
1815:
1809:
1808:
1803:
1802:
1800:
1798:
1794:
1779:
1775:
1772:(also called
1771:
1768:
1766:
1763:
1761:
1758:
1756:
1753:
1751:
1748:
1747:
1745:
1741:
1735:
1732:
1729:
1725:
1721:
1718:
1717:
1715:
1713:
1709:
1703:
1700:
1698:
1695:
1693:
1690:
1688:
1684:
1681:
1680:
1678:
1674:
1666:
1663:
1661:
1658:
1657:
1656:
1653:
1652:
1650:
1648:
1644:
1641:
1639:
1635:
1624:
1620:
1616:
1613:
1612:
1610:
1606:
1596:
1593:
1592:
1590:
1586:
1580:
1576:
1572:
1569:
1568:
1566:
1562:
1559:
1557:
1553:
1547:
1544:
1543:
1541:
1537:
1534:
1532:
1528:
1525:
1521:
1511:
1508:
1507:
1505:
1501:
1495:
1492:
1490:
1487:
1486:
1484:
1482:
1478:
1472:
1469:
1467:
1464:
1462:
1459:
1457:
1454:
1453:
1451:
1449:
1445:
1438:
1437:C-type lectin
1434:
1430:
1428:
1425:
1424:
1422:
1420:
1416:
1413:
1411:
1405:
1401:
1398:
1394:
1387:
1382:
1380:
1375:
1373:
1368:
1367:
1364:
1357:
1353:
1350:
1347:
1343:
1340:
1339:
1327:
1323:
1319:
1315:
1311:
1307:
1304:(2): 174–92.
1303:
1299:
1292:
1284:
1280:
1276:
1272:
1268:
1264:
1257:
1249:
1245:
1241:
1235:
1231:
1224:
1216:
1212:
1208:
1204:
1197:
1189:
1185:
1179:
1171:
1167:
1161:
1153:
1149:
1143:
1135:
1131:
1126:
1121:
1117:
1113:
1109:
1105:
1101:
1094:
1088:
1083:
1075:
1071:
1065:
1057:
1053:
1047:
1039:
1035:
1030:
1025:
1022:(2): 268–83.
1021:
1017:
1013:
1006:
998:
994:
990:
986:
982:
978:
973:
968:
964:
960:
956:
949:
941:
937:
933:
927:
923:
916:
914:
912:
910:
901:
897:
892:
887:
883:
879:
876:(4): 203–16.
875:
871:
867:
860:
858:
849:
845:
840:
835:
831:
827:
820:
812:
808:
804:
800:
796:
792:
789:(4): 271–82.
788:
784:
777:
763:on 2008-12-26
762:
758:
752:
748:
739:
736:
734:
731:
730:
724:
722:
721:polymorphisms
718:
714:
710:
700:
698:
694:
689:
685:
681:
677:
673:
659:
655:
653:
649:
645:
641:
637:
633:
629:
616:
613:
610:
606:
603:
600:
596:
592:
589:
586:
582:
578:
574:
570:
566:
562:
558:
554:
551:
548:
544:
541:
540:
539:
517:
513:
509:
505:
502:
500:
497:
495:
492:
491:
488:
484:
481:
479:
475:
472:
470:
467:
466:
463:
460:
458:
455:
453:
450:
449:
446:
443:
441:
438:
436:
433:
432:
429:
426:
424:
421:
419:
416:
415:
412:
409:
407:
404:
402:
400:
399:
391:
389:
378:
376:
372:
368:
358:
356:
352:
348:
344:
340:
335:
333:
322:
319:
311:
301:
297:
291:
290:
285:This section
283:
279:
274:
273:
265:
263:
259:
255:
251:
250:T helper cell
240:
238:
233:
231:
227:
223:
219:
209:
207:
201:
198:
194:
190:
180:
178:
173:
171:
167:
163:
159:
155:
151:
147:
142:
140:
136:
133:
129:
125:
121:
116:
114:
110:
106:
101:
99:
95:
91:
87:
83:
79:
75:
71:
67:
59:
56:
54:
50:
46:
42:
37:
30:
25:
20:
2263:MHC class II
2058:MHC class II
2057:
1804:
1712:Co-receptors
1665:MHC class II
1664:
1301:
1297:
1291:
1269:(3): 305–8.
1266:
1262:
1256:
1229:
1223:
1206:
1202:
1196:
1187:
1178:
1169:
1160:
1151:
1142:
1107:
1103:
1093:
1082:
1073:
1064:
1055:
1046:
1019:
1015:
1005:
962:
958:
948:
921:
873:
869:
829:
819:
786:
782:
776:
765:. Retrieved
761:the original
751:
713:heritability
706:
693:plasma cells
669:
625:
614:
604:
595:Small GTPase
590:
584:
580:
576:
568:
564:
560:
556:
552:
546:
542:
537:
410:
405:
401:
384:
364:
336:
329:
314:
305:
294:Please help
289:verification
286:
258:inflammation
246:
234:
222:interferon γ
215:
202:
193:heterodimers
186:
174:
143:
139:cell surface
120:phagocytosis
117:
102:
65:
64:
47:MHC Class II
22:MHC Class II
2212:Calgranulin
2015:MHC class I
1660:MHC class I
1556:Co-receptor
1419:Epsilon (ε)
1410:Fc receptor
1188:Entrez Gene
1170:Entrez Gene
1152:Entrez Gene
1074:Entrez Gene
1056:Entrez Gene
189:MHC class I
124:endocytosed
113:MHC class I
82:macrophages
39:Identifiers
2242:Categories
1564:stimulate:
767:2009-01-21
744:References
697:antibodies
682:Cells and
591:ARL14/ARF7
343:cathepsins
243:Importance
212:Expression
206:amino acid
53:Membranome
1503:Secretory
1448:Gamma (γ)
1248:986987876
981:0092-8674
940:820117219
688:cytokines
371:endosomes
308:June 2020
268:Synthesis
230:monocytes
183:Structure
128:lysosomes
2207:Arrestin
1851:KIR2DL5B
1846:KIR2DL5A
1588:inhibit:
1471:Neonatal
1326:26085603
1318:24752371
1283:17349258
1215:17513710
1134:14662749
1038:21458045
900:25720354
848:11983150
803:16557259
727:See also
583:xchange
516:HLA-DRB5
512:HLA-DRB4
508:HLA-DRB3
504:HLA-DRB1
487:HLA-DQB2
483:HLA-DQB1
478:HLA-DQA2
474:HLA-DQA1
462:HLA-DPB1
457:HLA-DPA1
132:epitopic
109:peptides
105:antigens
76:such as
2008:classes
1896:KIR3DS1
1891:KIR3DL3
1886:KIR3DL2
1881:KIR3DL1
1876:KIR2DS5
1871:KIR2DS4
1866:KIR2DS3
1861:KIR2DS2
1856:KIR2DS1
1841:KIR2DL4
1836:KIR2DL3
1831:KIR2DL2
1826:KIR2DL1
1770:ζ-chain
1647:Ligands
1638:T cells
1531:B cells
1466:FcγRIII
1125:2173613
997:8199773
989:8598037
891:6314495
717:Alleles
684:B cells
628:kinases
622:Pathway
571:) is a
547:PIP5K1A
499:HLA-DRA
445:HLA-DOB
440:HLA-DOA
428:HLA-DMB
423:HLA-DMA
262:B cells
162:HLA-DOB
158:HLA-DOA
94:B cells
84:, some
2149:HLA-DR
2117:HLA-DQ
2100:HLA-DP
2083:HLA-DO
2066:HLA-DM
1964:LILRB5
1959:LILRB4
1954:LILRB3
1949:LILRB2
1944:LILRB1
1939:LILRA6
1934:LILRA5
1929:LILRA4
1924:LILRA3
1919:LILRA2
1914:LILRA1
1494:Fcα/μR
1461:FcγRII
1433:FcεRII
1358:(MeSH)
1348:(MeSH)
1324:
1316:
1281:
1246:
1236:
1213:
1132:
1122:
1036:
995:
987:
979:
938:
928:
898:
888:
846:
811:131777
809:
801:
648:MHC-II
605:ARF7EP
543:PIK3R2
494:HLA-DR
469:HLA-DQ
452:HLA-DP
435:HLA-DO
418:HLA-DM
351:HLA-DM
170:HLA-DR
168:, and
166:HLA-DQ
154:HLA-DM
150:HLA-DP
92:, and
44:Symbol
2248:Genes
2185:Other
2048:HLA-G
2043:HLA-F
2038:HLA-E
2033:HLA-C
2028:HLA-B
2023:HLA-A
1489:FcαRI
1456:FcγRI
1427:FcεRI
1322:S2CID
993:S2CID
807:S2CID
644:actin
640:MYO1E
615:MYO1E
609:MYO1E
593:is a
406:Alpha
394:Genes
226:CIITA
187:Like
1805:see
1778:TCRζ
1776:and
1774:CD3ζ
1765:CD3ε
1760:CD3δ
1755:CD3γ
1728:CD8β
1726:and
1724:CD8α
1702:TRG@
1697:TRD@
1692:TRB@
1687:TRA@
1623:CD79
1619:Ig-β
1615:Ig-α
1595:CD22
1579:CD81
1575:CD19
1571:CD21
1314:PMID
1279:PMID
1244:OCLC
1234:ISBN
1211:PMID
1130:PMID
1034:PMID
1016:Cell
985:PMID
977:ISSN
959:Cell
936:OCLC
926:ISBN
896:PMID
844:PMID
830:Cell
799:PMID
563:ec7
553:PSD4
545:and
411:Beta
355:CLIP
347:CLIP
103:The
1750:CD3
1734:CD4
1720:CD8
1683:TCR
1655:MHC
1546:BCR
1435:is
1306:doi
1271:doi
1207:178
1120:PMC
1112:doi
1108:163
1024:doi
1020:145
967:doi
886:PMC
878:doi
834:doi
791:doi
680:CD8
676:CD4
573:GEF
298:by
254:CD4
197:HLA
115:).
2244::
2174:β5
2169:β4
2164:β3
2159:β1
2142:β3
2137:β2
2132:β1
2127:α2
2122:α1
2110:β1
2105:α1
1685::
1395::
1320:.
1312:.
1302:47
1300:.
1277:.
1267:66
1242:.
1205:.
1186:.
1168:.
1150:.
1128:.
1118:.
1106:.
1102:.
1072:.
1054:.
1032:.
1018:.
1014:.
991:.
983:.
975:.
963:84
961:.
957:.
934:.
908:^
894:.
884:.
874:15
872:.
868:.
856:^
842:.
828:.
805:.
797:.
785:.
715:.
514:,
510:,
506:,
485:,
476:,
264:.
239:.
172:.
164:,
160:,
156:,
152:,
141:.
100:.
88:,
80:,
58:63
2154:α
2093:β
2088:α
2076:β
2071:α
1998:e
1991:t
1984:v
1780:)
1730:)
1625:)
1621:(
1617:/
1577:/
1573:/
1439:)
1431:(
1385:e
1378:t
1371:v
1328:.
1308::
1285:.
1273::
1250:.
1217:.
1190:.
1172:.
1154:.
1136:.
1114::
1076:.
1058:.
1040:.
1026::
999:.
969::
942:.
902:.
880::
850:.
836::
813:.
793::
787:6
770:.
611:.
601:.
585:F
581:E
577:G
575:(
569:4
565:D
561:S
557:P
555:(
321:)
315:(
310:)
306:(
292:.
252:(
Text is available under the Creative Commons Attribution-ShareAlike License. Additional terms may apply.
