| Structural highlights
Disease
HLAA_HUMAN Selection of immunotherapy in solid cancer;Birdshot chorioretinopathy;Prediction of phenytoin or carbamazepine toxicity. Alleles A*02:01 and A*24:02 are associated with increased susceptibility to diabetes mellitus, insulin-dependent (IDDM) (PubMed:22245737, PubMed:18802479, PubMed:16731854, PubMed:22522618). In a glucose-dependent way, allele A*02:01 may aberrantly present the signal peptide of preproinsulin (ALWGPDPAAA) on the surface of pancreatic beta cells to autoreactive CD8-positive T cells, potentially driving T-cell mediated cytotoxicity in pancreatic islets (PubMed:22245737, PubMed:18802479). Allele A*24:02 may present the signal peptide of preproinsulin (LWMRLLPLL) and contribute to acute pancreatic beta-cell destruction and early onset of IDDM (PubMed:16731854, PubMed:22522618).[1] [2] [3] [4] Allele A*03:01 is associated with increased susceptibility to multiple sclerosis (MS), an autoimmune disease of the central nervous system (PubMed:10746785). May contribute to the initiation phase of the disease by presenting myelin PLP1 self-peptide (KLIETYFSK) to autoreactive CD8-positive T cells capable of initiating the first autoimmune attacks (PubMed:18953350).[5] [6] Allele A*26:01 is associated with increased susceptibility to Behcet disease (BD) in the Northeast Asian population. Especially in the HLA-B*51-negative BD populations, HLA-A*26 is significantly associated with the onset of BD.[7] Allele A*29:02 is associated with increased susceptibility to birdshot chorioretinopathy (BSCR). May aberrantly present retinal autoantigens and induce autoimmune uveitis.[8]
Function
HLAA_HUMAN Antigen-presenting major histocompatibility complex class I (MHCI) molecule. In complex with B2M/beta 2 microglobulin displays primarily viral and tumor-derived peptides on antigen-presenting cells for recognition by alpha-beta T cell receptor (TCR) on HLA-A-restricted CD8-positive T cells, guiding antigen-specific T cell immune response to eliminate infected or transformed cells (PubMed:2456340, PubMed:2784196, PubMed:1402688, PubMed:7504010, PubMed:9862734, PubMed:10449296, PubMed:12138174, PubMed:12393434, PubMed:15893615, PubMed:17189421, PubMed:19543285, PubMed:21498667, PubMed:24192765, PubMed:7694806, PubMed:24395804, PubMed:28250417). May also present self-peptides derived from the signal sequence of secreted or membrane proteins, although T cells specific for these peptides are usually inactivated to prevent autoreactivity (PubMed:25880248, PubMed:7506728, PubMed:7679507). Both the peptide and the MHC molecule are recognized by TCR, the peptide is responsible for the fine specificity of antigen recognition and MHC residues account for the MHC restriction of T cells (PubMed:12796775, PubMed:18275829, PubMed:19542454, PubMed:28250417). Typically presents intracellular peptide antigens of 8 to 13 amino acids that arise from cytosolic proteolysis via IFNG-induced immunoproteasome or via endopeptidase IDE/insulin-degrading enzyme (PubMed:17189421, PubMed:20364150, PubMed:17079320, PubMed:26929325, PubMed:27049119). Can bind different peptides containing allele-specific binding motifs, which are mainly defined by anchor residues at position 2 and 9 (PubMed:7504010, PubMed:9862734).[9] [10] [11] [12] [13] [14] [15] [16] [17] [18] [19] [20] [21] [22] [23] [24] [25] [26] [27] [28] [29] [30] [31] [32] [33] [34] Allele A*01:01: Presents a restricted peptide repertoire including viral epitopes derived from IAV NP/nucleoprotein (CTELKLSDY), IAV PB1/polymerase basic protein 1 (VSDGGPNLY), HAdV-11 capsid L3/hexon protein (LTDLGQNLLY), SARS-CoV-2 3a/ORF3a (FTSDYYQLY) as well as tumor peptide antigens including MAGE1 (EADPTGHSY), MAGEA3 (EVDPIGHLY) and WT1 (TSEKRPFMCAY), all having in common a canonical motif with a negatively charged Asp or Glu residue at position 3 and a Tyr anchor residue at the C-terminus (PubMed:1402688, PubMed:7504010, PubMed:17189421, PubMed:20364150, PubMed:25880248, PubMed:30530481, PubMed:19177349, PubMed:24395804, PubMed:26758806, PubMed:32887977). A number of HLA-A*01:01-restricted peptides carry a post-translational modification with oxidation and N-terminal acetylation being the most frequent (PubMed:25880248). Fails to present highly immunogenic peptides from the EBV latent antigens (PubMed:18779413).[35] [36] [37] [38] [39] [40] [41] [42] [43] [44] Allele A*02:01: A major allele in human populations, presents immunodominant viral epitopes derived from IAV M/matrix protein 1 (GILGFVFTL), HIV-1 env (TLTSCNTSV), HIV-1 gag-pol (ILKEPVHGV), HTLV-1 Tax (LLFGYPVYV), HBV C/core antigen (FLPSDFFPS), HCMV UL83/pp65 (NLVPMVATV) as well as tumor peptide antigens including MAGEA4 (GVYDGREHTV), WT1 (RMFPNAPYL) and CTAG1A/NY-ESO-1 (SLLMWITQC), all having in common hydrophobic amino acids at position 2 and at the C-terminal anchors.[45] [46] [47] [48] [49] [50] [51] [52] [53] [54] [55] [56] [57] [58] [59] [60] [61] Allele A*03:01: Presents viral epitopes derived from IAV NP (ILRGSVAHK), HIV-1 nef (QVPLRPMTYK), HIV-1 gag-pol (AIFQSSMTK), SARS-CoV-2 N/nucleoprotein (KTFPPTEPK) as well as tumor peptide antigens including PMEL (LIYRRRLMK), NODAL (HAYIQSLLK), TRP-2 (RMYNMVPFF), all having in common hydrophobic amino acids at position 2 and Lys or Arg anchor residues at the C-terminus (PubMed:7504010, PubMed:7679507, PubMed:9862734, PubMed:19543285, PubMed:21943705, PubMed:2456340, PubMed:32887977). May also display spliced peptides resulting from the ligation of two separate proteasomal cleavage products that are not contiguous in the parental protein (PubMed:27049119).[62] [63] [64] [65] [66] [67] [68] Allele A*11:01: Presents several immunodominant epitopes derived from HIV-1 gag-pol and HHV-4 EBNA4, containing the peptide motif with Val, Ile, Thr, Leu, Tyr or Phe at position 2 and Lys anchor residue at the C-terminus. Important in the control of HIV-1, EBV and HBV infections (PubMed:10449296). Presents an immunodominant epitope derived from SARS-CoV-2 N/nucleoprotein (KTFPPTEPK) (PubMed:32887977).[69] [70] Allele A*23:01: Interacts with natural killer (NK) cell receptor KIR3DL1 and may contribute to functional maturation of NK cells and self-nonself discrimination during innate immune response.[71] Allele A*24:02: Presents viral epitopes derived from HIV-1 nef (RYPLTFGWCF), EBV lytic- and latent-cycle antigens BRLF1 (TYPVLEEMF), BMLF1 (DYNFVKQLF) and LMP2 (IYVLVMLVL), SARS-CoV nucleocapsid/N (QFKDNVILL), as well as tumor peptide antigens including PRAME (LYVDSLFFL), all sharing a common signature motif, namely an aromatic residue Tyr or Phe at position 2 and a nonhydrophobic anchor residue Phe, Leu or Iso at the C-terminus (PubMed:9047241, PubMed:12393434, PubMed:24192765, PubMed:20844028). Interacts with natural killer (NK) cell receptor KIR3DL1 and may contribute to functional maturation of NK cells and self-nonself discrimination during innate immune response (PubMed:17182537, PubMed:18502829).[72] [73] [74] [75] [76] [77] Allele A*26:01: Presents several epitopes derived from HIV-1 gag-pol (EVIPMFSAL, ETKLGKAGY) and env (LVSDGGPNLY), carrying as anchor residues preferentially Glu at position 1, Val or Thr at position 2 and Tyr at the C-terminus.[78] Allele A*29:02: Presents peptides having a common motif, namely a Glu residue at position 2 and Tyr or Leu anchor residues at the C-terminus.[79] Allele A*32:01: Interacts with natural killer (NK) cell receptor KIR3DL1 and may contribute to functional maturation of NK cells and self-nonself discrimination during innate immune response.[80] Allele A*68:01: Presents viral epitopes derived from IAV NP (KTGGPIYKR) and HIV-1 tat (ITKGLGISYGR), having a common signature motif namely, Val or Thr at position 2 and positively charged residues Arg or Lys at the C-terminal anchor.[81] [82] [83] Allele A*74:01: Presents immunodominant HIV-1 epitopes derived from gag-pol (GQMVHQAISPR, QIYPGIKVR) and rev (RQIHSISER), carrying an aliphatic residue at position 2 and Arg anchor residue at the C-terminus. May contribute to viral load control in chronic HIV-1 infection.[84]
Publication Abstract from PubMed
Adoptive cell therapy with tumor-specific T cells can mediate durable cancer regression. The prime target of tumor-specific T cells are neoantigens arising from mutations in self-proteins during malignant transformation. To understand T cell recognition of cancer neoantigens at the atomic level, we studied oligoclonal T cell receptors (TCRs) that recognize a neoepitope arising from a driver mutation in the p53 oncogene (p53R175H) presented by the major histocompatibility complex class I molecule HLA-A2. We previously reported the structures of three p53R175H-specific TCRs (38-10, 12-6, and 1a2) bound to p53R175H and HLA-A2. The structures showed that these TCRs discriminate between WT and mutant p53 by forming extensive interactions with the R175H mutation. Here, we report the structure of a fourth p53R175H-specific TCR (6-11) in complex with p53R175H and HLA-A2. In contrast to 38-10, 12-6, and 1a2, TCR 6-11 makes no direct contacts with the R175H mutation, yet is still able to distinguish mutant from WT p53. Structure-based in silico mutagenesis revealed that the 60-fold loss in 6-11 binding affinity for WT p53 compared to p53R175H is mainly due to the higher energetic cost of desolvating R175 in the WT p53 peptide during complex formation than H175 in the mutant. This indirect strategy for preferential neoantigen recognition by 6-11 is fundamentally different from the direct strategies employed by other TCRs and highlights the multiplicity of solutions to recognizing p53R175H with sufficient selectivity to mediate T cell killing of tumor but not normal cells.
T cell receptors employ diverse strategies to target a p53 cancer neoantigen.,Wu D, Gowathaman R, Pierce BG, Mariuzza RA J Biol Chem. 2022 Mar;298(3):101684. doi: 10.1016/j.jbc.2022.101684. Epub 2022 , Feb 3. PMID:35124005[85]
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
See Also
References
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- ↑ Skowera A, Ellis RJ, Varela-Calvino R, Arif S, Huang GC, Van-Krinks C, Zaremba A, Rackham C, Allen JS, Tree TI, Zhao M, Dayan CM, Sewell AK, Unger WW, Drijfhout JW, Ossendorp F, Roep BO, Peakman M. CTLs are targeted to kill beta cells in patients with type 1 diabetes through recognition of a glucose-regulated preproinsulin epitope. J Clin Invest. 2008 Oct;118(10):3390-402. doi: 10.1172/JCI35449. PMID:18802479 doi:http://dx.doi.org/10.1172/JCI35449
- ↑ Bulek AM, Cole DK, Skowera A, Dolton G, Gras S, Madura F, Fuller A, Miles JJ, Gostick E, Price DA, Drijfhout JW, Knight RR, Huang GC, Lissin N, Molloy PE, Wooldridge L, Jakobsen BK, Rossjohn J, Peakman M, Rizkallah PJ, Sewell AK. Structural basis for the killing of human beta cells by CD8(+) T cells in type 1 diabetes. Nat Immunol. 2012 Jan 15. doi: 10.1038/ni.2206. PMID:22245737 doi:10.1038/ni.2206
- ↑ Kronenberg D, Knight RR, Estorninho M, Ellis RJ, Kester MG, de Ru A, Eichmann M, Huang GC, Powrie J, Dayan CM, Skowera A, van Veelen PA, Peakman M. Circulating preproinsulin signal peptide-specific CD8 T cells restricted by the susceptibility molecule HLA-A24 are expanded at onset of type 1 diabetes and kill beta-cells. Diabetes. 2012 Jul;61(7):1752-9. doi: 10.2337/db11-1520. Epub 2012 Apr 20. PMID:22522618 doi:http://dx.doi.org/10.2337/db11-1520
- ↑ Fogdell-Hahn A, Ligers A, Gronning M, Hillert J, Olerup O. Multiple sclerosis: a modifying influence of HLA class I genes in an HLA class II associated autoimmune disease. Tissue Antigens. 2000 Feb;55(2):140-8. doi: 10.1034/j.1399-0039.2000.550205.x. PMID:10746785 doi:http://dx.doi.org/10.1034/j.1399-0039.2000.550205.x
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- ↑ Traversari C, van der Bruggen P, Luescher IF, Lurquin C, Chomez P, Van Pel A, De Plaen E, Amar-Costesec A, Boon T. A nonapeptide encoded by human gene MAGE-1 is recognized on HLA-A1 by cytolytic T lymphocytes directed against tumor antigen MZ2-E. J Exp Med. 1992 Nov 1;176(5):1453-7. doi: 10.1084/jem.176.5.1453. PMID:1402688 doi:http://dx.doi.org/10.1084/jem.176.5.1453
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- ↑ Asemissen AM, Keilholz U, Tenzer S, Muller M, Walter S, Stevanovic S, Schild H, Letsch A, Thiel E, Rammensee HG, Scheibenbogen C. Identification of a highly immunogenic HLA-A*01-binding T cell epitope of WT1. Clin Cancer Res. 2006 Dec 15;12(24):7476-82. doi: 10.1158/1078-0432.CCR-06-1337. PMID:17189421 doi:http://dx.doi.org/10.1158/1078-0432.CCR-06-1337
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- ↑ Hadrup SR, Bakker AH, Shu CJ, Andersen RS, van Veluw J, Hombrink P, Castermans E, Thor Straten P, Blank C, Haanen JB, Heemskerk MH, Schumacher TN. Parallel detection of antigen-specific T-cell responses by multidimensional encoding of MHC multimers. Nat Methods. 2009 Jul;6(7):520-6. doi: 10.1038/nmeth.1345. Epub 2009 Jun 21. PMID:19543285 doi:http://dx.doi.org/10.1038/nmeth.1345
- ↑ Parmentier N, Stroobant V, Colau D, de Diesbach P, Morel S, Chapiro J, van Endert P, Van den Eynde BJ. Production of an antigenic peptide by insulin-degrading enzyme. Nat Immunol. 2010 May;11(5):449-54. doi: 10.1038/ni.1862. Epub 2010 Apr 4. PMID:20364150 doi:http://dx.doi.org/10.1038/ni.1862
- ↑ Matthews PC, Adland E, Listgarten J, Leslie A, Mkhwanazi N, Carlson JM, Harndahl M, Stryhn A, Payne RP, Ogwu A, Huang KH, Frater J, Paioni P, Kloverpris H, Jooste P, Goedhals D, van Vuuren C, Steyn D, Riddell L, Chen F, Luzzi G, Balachandran T, Ndung'u T, Buus S, Carrington M, Shapiro R, Heckerman D, Goulder PJ. HLA-A*7401-mediated control of HIV viremia is independent of its linkage disequilibrium with HLA-B*5703. J Immunol. 2011 May 15;186(10):5675-86. doi: 10.4049/jimmunol.1003711. Epub 2011 , Apr 15. PMID:21498667 doi:http://dx.doi.org/10.4049/jimmunol.1003711
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- ↑ Quinones-Parra S, Grant E, Loh L, Nguyen TH, Campbell KA, Tong SY, Miller A, Doherty PC, Vijaykrishna D, Rossjohn J, Gras S, Kedzierska K. Preexisting CD8+ T-cell immunity to the H7N9 influenza A virus varies across ethnicities. Proc Natl Acad Sci U S A. 2014 Jan 21;111(3):1049-54. doi:, 10.1073/pnas.1322229111. Epub 2014 Jan 6. PMID:24395804 doi:http://dx.doi.org/10.1073/pnas.1322229111
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- ↑ Giam K, Ayala-Perez R, Illing PT, Schittenhelm RB, Croft NP, Purcell AW, Dudek NL. A comprehensive analysis of peptides presented by HLA-A1. Tissue Antigens. 2015 Jun;85(6):492-6. doi: 10.1111/tan.12565. Epub 2015 Apr 16. PMID:25880248 doi:http://dx.doi.org/10.1111/tan.12565
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- ↑ DiBrino M, Tsuchida T, Turner RV, Parker KC, Coligan JE, Biddison WE. HLA-A1 and HLA-A3 T cell epitopes derived from influenza virus proteins predicted from peptide binding motifs. J Immunol. 1993 Dec 1;151(11):5930-5. PMID:7504010
- ↑ DiBrino M, Parker KC, Shiloach J, Turner RV, Tsuchida T, Garfield M, Biddison WE, Coligan JE. Endogenous peptides with distinct amino acid anchor residue motifs bind to HLA-A1 and HLA-B8. J Immunol. 1994 Jan 15;152(2):620-31. PMID:7506728
- ↑ DiBrino M, Parker KC, Shiloach J, Knierman M, Lukszo J, Turner RV, Biddison WE, Coligan JE. Endogenous peptides bound to HLA-A3 possess a specific combination of anchor residues that permit identification of potential antigenic peptides. Proc Natl Acad Sci U S A. 1993 Feb 15;90(4):1508-12. doi: 10.1073/pnas.90.4.1508. PMID:7679507 doi:http://dx.doi.org/10.1073/pnas.90.4.1508
- ↑ Madden DR, Garboczi DN, Wiley DC. The antigenic identity of peptide-MHC complexes: a comparison of the conformations of five viral peptides presented by HLA-A2. Cell. 1993 Nov 19;75(4):693-708. PMID:7694806
- ↑ Kawakami Y, Robbins PF, Wang X, Tupesis JP, Parkhurst MR, Kang X, Sakaguchi K, Appella E, Rosenberg SA. Identification of new melanoma epitopes on melanosomal proteins recognized by tumor infiltrating T lymphocytes restricted by HLA-A1, -A2, and -A3 alleles. J Immunol. 1998 Dec 15;161(12):6985-92. PMID:9862734
- ↑ Traversari C, van der Bruggen P, Luescher IF, Lurquin C, Chomez P, Van Pel A, De Plaen E, Amar-Costesec A, Boon T. A nonapeptide encoded by human gene MAGE-1 is recognized on HLA-A1 by cytolytic T lymphocytes directed against tumor antigen MZ2-E. J Exp Med. 1992 Nov 1;176(5):1453-7. doi: 10.1084/jem.176.5.1453. PMID:1402688 doi:http://dx.doi.org/10.1084/jem.176.5.1453
- ↑ Asemissen AM, Keilholz U, Tenzer S, Muller M, Walter S, Stevanovic S, Schild H, Letsch A, Thiel E, Rammensee HG, Scheibenbogen C. Identification of a highly immunogenic HLA-A*01-binding T cell epitope of WT1. Clin Cancer Res. 2006 Dec 15;12(24):7476-82. doi: 10.1158/1078-0432.CCR-06-1337. PMID:17189421 doi:http://dx.doi.org/10.1158/1078-0432.CCR-06-1337
- ↑ Brennan RM, Burrows SR. A mechanism for the HLA-A*01-associated risk for EBV+ Hodgkin lymphoma and infectious mononucleosis. Blood. 2008 Sep 15;112(6):2589-90. doi: 10.1182/blood-2008-06-162883. PMID:18779413 doi:http://dx.doi.org/10.1182/blood-2008-06-162883
- ↑ Kumar P, Vahedi-Faridi A, Saenger W, Ziegler A, Uchanska-Ziegler B. Conformational changes within the HLA-A1:MAGE-A1 complex induced by binding of a recombinant antibody fragment with TCR-like specificity. Protein Sci. 2009 Jan;18(1):37-49. PMID:19177349 doi:10.1002/pro.4
- ↑ Parmentier N, Stroobant V, Colau D, de Diesbach P, Morel S, Chapiro J, van Endert P, Van den Eynde BJ. Production of an antigenic peptide by insulin-degrading enzyme. Nat Immunol. 2010 May;11(5):449-54. doi: 10.1038/ni.1862. Epub 2010 Apr 4. PMID:20364150 doi:http://dx.doi.org/10.1038/ni.1862
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