HLA‐B27: a registry of constitutive peptide ligands

Wiley - Tập 63 Số 5 - Trang 424-445 - 2004
José A. Łópez de Castro1, Iñaki Álvarez1, Miguel Marcilla1, Alberto Paradela1, Manuel Ramos1, L. G. Sesma1, Miriam Vázquez1
1Centro de Biología Molecular Severo Ochoa (Consejo Superior de Investigaciones Científicas and Universidad Autónoma de Madrid), Universidad Autónoma, Madrid, Spain

Tóm tắt

Abstract:  The very strong association of human leukocyte antigen (HLA)‐B27 with spondyloarthritis might be related to its peptide‐presenting properties. The natural polymorphism of this molecule influences both peptide specificity and disease susceptibility. In this study, we present a comprehensive compilation of known natural ligands of HLA‐B27 arising from endogenous proteins of human cells, together with a statistical assessment of residue usage among constitutive peptide repertoires of multiple HLA‐B27 subtypes. This analysis provides evidence that every peptide position, including ‘non‐anchor’ ones, may be subjected to selection on the basis of its contribution to HLA‐B27 binding and also allows a quantization of residue preferences at known anchor positions. The present registry is intended as a basis on which to build up reliable criteria to assess the effect of HLA‐B27 polymorphism on peptide presentation, for T‐cell epitope predictions, and for molecular mimicry studies.

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Tài liệu tham khảo

10.1016/0167-5699(90)90051-A

10.1034/j.1399-0039.2002.600301.x

10.1038/353326a0

10.1016/0092-8674(92)90252-8

10.1074/jbc.M108882200

10.1111/j.1399-0039.1997.tb02805.x

10.1016/1074-7613(94)90105-8

10.1172/JCI119102

Griffin TA, 1997, Naturally occurring A pocket polymorphism in HLA‐B*2703 increases the dependence on an accessory anchor residue at P1 for optimal binding of nonamer peptides, J Immunol, 159, 4887, 10.4049/jimmunol.159.10.4887

10.1074/jbc.M200371200

10.1146/annurev.immunol.17.1.739

10.1002/1439-7633(20000703)1:1<16::AID-CBIC16>3.0.CO;2-Y

10.4049/jimmunol.166.2.1016

10.4049/jimmunol.164.12.6120

10.1074/jbc.M308816200

10.1084/jem.192.12.1755

10.1038/353321a0

10.1074/jbc.M206392200

10.1074/jbc.M307457200

10.1016/0092-8674(93)90472-3

10.1146/annurev.iy.13.040195.003103

10.1038/360364a0

Del Porto P, 1994, Identification of a novel HLA‐B27 subtype by restriction analysis of a cytotoxic gamma delta T cell clone, J Immunol, 153, 3093, 10.4049/jimmunol.153.7.3093

10.1002/eji.1830270205

Uchanska‐Ziegler B, 2004, HLA 2002. Immunobiology of the Human MHC

10.1074/jbc.M204155200

Vega MA, 1985, Delineation of functional sites in HLA‐B27 antigens. Molecular analysis of HLA‐B27 variant Wewak I defined by cytolytic T lymphocytes, J Immunol, 135, 3323, 10.4049/jimmunol.135.5.3323

10.1007/BF00176678

Vega MA, 1986, Molecular analysis of a functional subtype of HLA‐B27. A possible evolutionary pathway for HLA‐B27 polymorphism, J Immunol, 137, 3557, 10.4049/jimmunol.137.11.3557

10.1007/BF00241265

10.1111/j.1399-0039.1997.tb02741.x

Rojo S, 1987, Structural analysis of an HLA‐B27 functional variant, B27d, detected in American blacks, J Immunol, 139, 3396, 10.4049/jimmunol.139.10.3396

10.1016/0198-8859(88)90072-9

10.1002/eji.1830250837

10.1016/S0198-8859(02)00364-6

10.1016/S1074-7613(02)00304-7

10.4049/jimmunol.170.2.961

10.1126/science.283.5406.1335

10.1007/BF00171803

Paradela A, 1998, The same natural ligand is involved in allorecognition of multiple HLA‐B27 subtypes by a single T cell clone: role of peptide and the MHC molecule in alloreactivity, J Immunol, 161, 5481, 10.4049/jimmunol.161.10.5481

10.4049/jimmunol.167.3.1212

10.1002/1529-0131(199909)42:9<1975::AID-ANR25>3.0.CO;2-V

10.4049/jimmunol.164.1.329

10.1074/jbc.M104663200

10.1074/jbc.M205470200

10.1111/j.1399-0039.1997.tb02705.x

10.1034/j.1399-0039.2001.580603.x

10.1007/s002510050334

10.1111/j.1399-0039.1998.tb02941.x