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Journal articles on the topic 'HLA region'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Sachs, J. A., D. Jaraquemada, and H. Festenstein. "Intra HLA-D Region Recombinant Maps HLA-DR between HLA-B and HLA-D." Tissue Antigens 17, no. 1 (December 11, 2008): 43–56. http://dx.doi.org/10.1111/j.1399-0039.1981.tb00665.x.

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2

Lin, Ling, Marcel Hungs, and Emmanuel Mignot. "Narcolepsy and the HLA region." Journal of Neuroimmunology 117, no. 1-2 (July 2001): 9–20. http://dx.doi.org/10.1016/s0165-5728(01)00333-2.

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3

Mason, P. M., and P. Parham. "HLA class I region sequences, 1998." Tissue Antigens 51, no. 4 (September 30, 2008): 417–66. http://dx.doi.org/10.1111/j.1399-0039.1998.tb02983.x.

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4

Marsh, S. G. E. "HLA class II region sequences, 1998." Tissue Antigens 51, no. 4 (September 30, 2008): 467–507. http://dx.doi.org/10.1111/j.1399-0039.1998.tb02984.x.

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5

Leder, Richard O., and Susan E. Hodge. "Psoriasis Linkage in the HLA Region." American Journal of Human Genetics 64, no. 3 (March 1999): 895. http://dx.doi.org/10.1086/302290.

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6

GERAGHTY, DANIEL E., MARTA JANER, and THIERRY GUILLAUDEUX. "NEW GENES IN THE HLA REGION." Vox Sanguinis 70, S3 (January 1996): 95–101. http://dx.doi.org/10.1111/j.1423-0410.1996.tb01379.x.

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7

Bach, Fritz H. "The HLA class II genes and products: the HLA-D region." Immunology Today 6, no. 3 (March 1985): 89–94. http://dx.doi.org/10.1016/0167-5699(85)90023-4.

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8

Pei, Ji, S. Yoon Choo, Thomas Spies, Jack L. Strominger, and John A. Hansen. "Association of four HLA class III region genomic markers with HLA haplotypes." Tissue Antigens 37, no. 5 (May 1991): 191–96. http://dx.doi.org/10.1111/j.1399-0039.1991.tb01871.x.

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9

Momigliano Richiardi, Patricia, Sandra D’Alfonso, and Nazario Cappello. "Association of microsatellites in the HLA central region and HLA extended haplotypes." Human Immunology 47, no. 1-2 (April 1996): 6. http://dx.doi.org/10.1016/0198-8859(96)84705-7.

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10

Fiorentino, Francesco, Semra Kahraman, Hüseyin Karadayi, Anil Biricik, Semra Sertyel, Güvenc Karlikaya, Yaman Saglam, Daniele Podini, Andrea Nuccitelli, and Marina Baldi. "Short tandem repeats haplotyping of the HLA region in preimplantation HLA matching." European Journal of Human Genetics 13, no. 8 (May 11, 2005): 953–58. http://dx.doi.org/10.1038/sj.ejhg.5201435.

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11

Foissac, A., M. Salhi, and A. Cambon-Thomsen. "Microsatellites in the HLA region: 1999 update." Tissue Antigens 55, no. 6 (June 2000): 477–509. http://dx.doi.org/10.1034/j.1399-0039.2000.550601.x.

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12

Marsh, Steven G. E., and Julia G. Bodmer. "HLA Class II region nucleotide sequences, 1995." Tissue Antigens 46, no. 3 (September 1995): 258–80. http://dx.doi.org/10.1111/j.1399-0039.1995.tb03125.x.

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13

Feichtlbauer, P., M. Gomolka, G. Brünnler, T. Eisenhut, H. Truckenbrodt, and E. D. Albert. "HLA region microsatellite polymorphisms in juvenile arthritis." Tissue Antigens 52, no. 3 (September 1998): 220–29. http://dx.doi.org/10.1111/j.1399-0039.1998.tb03036.x.

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14

Foissac, A., and A. Cambon-Thomsen. "Microsatellites in the HLA region: 1998 update." Tissue Antigens 52, no. 4 (October 1998): 318–52. http://dx.doi.org/10.1111/j.1399-0039.1998.tb03054.x.

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15

Marsh, S. G. E., and J. G. Bodmer. "HLA CLASS II REGION NUCLEOTIDE SEQUENCES, 1994." European Journal of Immunogenetics 21, no. 6 (December 1994): 519–51. http://dx.doi.org/10.1111/j.1744-313x.1994.tb00223.x.

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16

Goris, A. "Comment: The HLA region in multiple sclerosis." Neurology 79, no. 6 (August 7, 2012): 544. http://dx.doi.org/10.1212/wnl.0b013e318263c45b.

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17

Neale, B. M. "Harvesting HLA Region for Multiple Sclerosis Effects." Science Translational Medicine 5, no. 215 (December 11, 2013): 215ec206. http://dx.doi.org/10.1126/scitranslmed.3008081.

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18

Trowsdale, John, and R. Duncan Campbell. "Physical map of the human HLA region." Immunology Today 9, no. 2 (January 1988): 34–35. http://dx.doi.org/10.1016/0167-5699(88)91250-9.

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19

Yao, Z., Andrea Volgger, Siegfried Scholz, and Ekkehard Albert. "Polymorphism of the HLA-C promotor region." Immunogenetics 45, no. 6 (April 9, 1997): 428–31. http://dx.doi.org/10.1007/s002510050225.

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20

Andersson, Göran. "Evolution of the human HLA-DR region." Frontiers in Bioscience 3, no. 4 (1998): d739–745. http://dx.doi.org/10.2741/a317.

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21

Trowsdale, J. "The human HLA-D region — A summary." Veterinary Immunology and Immunopathology 17, no. 1-4 (December 1987): 223–30. http://dx.doi.org/10.1016/0165-2427(87)90142-5.

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22

Solier, Corinne, Valérie Mallet, Françoise Lenfant, Arnaud Bertrand, Anne Huchenq, and Philippe Le Bouteiller. "HLA-G unique promoter region: functional implications." Immunogenetics 53, no. 8 (October 1, 2001): 617–25. http://dx.doi.org/10.1007/s00251-001-0373-0.

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23

Tate, Genshu, and Mitsugu Ishizawa. "Structural Similarity of the HLA-DQ Region in DQ3 and DQ4 Haplotypes and Structural Diversity of the HLA-DQ Region in HLA-DR7 Haplotypes." Microbiology and Immunology 36, no. 7 (July 1992): 737–44. http://dx.doi.org/10.1111/j.1348-0421.1992.tb02076.x.

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24

Torres, Anthony R., Jonna B. Westover, and Allen J. Rosenspire. "HLA Immune Function Genes in Autism." Autism Research and Treatment 2012 (2012): 1–13. http://dx.doi.org/10.1155/2012/959073.

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The human leukocyte antigen (HLA) genes on chromosome 6 are instrumental in many innate and adaptive immune responses. The HLA genes/haplotypes can also be involved in immune dysfunction and autoimmune diseases. It is now becoming apparent that many of the non-antigen-presenting HLA genes make significant contributions to autoimmune diseases. Interestingly, it has been reported that autism subjects often have associations with HLA genes/haplotypes, suggesting an underlying dysregulation of the immune system mediated by HLA genes. Genetic studies have only succeeded in identifying autism-causing genes in a small number of subjects suggesting that the genome has not been adequately interrogated. Close examination of the HLA region in autism has been relatively ignored, largely due to extraordinary genetic complexity. It is our proposition that genetic polymorphisms in the HLA region, especially in the non-antigen-presenting regions, may be important in the etiology of autism in certain subjects.

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25

Kennedy, Amy E., Sandeep K. Singh, Malaroviyam Samikkannu, and M. Tevfik Dorak. "184-P Correlations of complex disease-associated HLA region SNPs with HLA alleles." Human Immunology 72 (October 2011): S133. http://dx.doi.org/10.1016/j.humimm.2011.07.209.

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26

Choppin, J., J. J. Metzger, M. Bouillot, J. P. Briand, F. Connan, M. H. Van Regenmortel, and J. P. Levy. "Recognition of HLA class I molecules by antisera directed to synthetic peptides corresponding to different regions of the HLA-B7 heavy chain." Journal of Immunology 136, no. 5 (March 1, 1986): 1738–44. http://dx.doi.org/10.4049/jimmunol.136.5.1738.

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Abstract Antisera have been prepared in rabbits and in mice against different peptides corresponding to four hydrophilic and variable regions of HLA-B7 heavy chain (65-82, 99-118, 138-157, and 164-187). Specific antipeptide sera have been obtained with all synthetic peptides; for three of them which were more than 20 amino acids long, highly potent sera were elicited by injection of the free peptide. Three overlapping peptides included in region 138-157 have been used, and two different antigenic sites were detected in this region. HLA molecules solubilized in nonionic detergent were precipitated by antipeptide sera directed against regions 65-82, 138-157, and 164-187, but not by antipeptide serum directed against the less hydrophilic region 99-118. Analysis by two-dimensional electrophoresis of the isolated molecules confirmed the anti-HLA specificity of the antipeptide 65-82 and 138-157 sera. Variable numbers of HLA-related spots were found according to the antisera used. Antipeptide 138-157 serum precipitated numerous HLA molecules and therefore probably reacted with monomorphic determinants whereas antipeptide 65-82 appeared specific for a more limited number of HLA antigens. Such reagents directed against well-defined regions of the HLA class I heavy chain are of considerable interest, notably for the mapping of antigenic epitopes on the molecule and for the study of relationships between structure and function.

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27

Harty, Lea C., Albert Y. Lin, Alisa M. Goldstein, Elaine S. Jaffe, Mary Carrington, Margaret A. Tucker, and William S. Modi. "HLA-DR, HLA-DQ, and TAP genes in familial Hodgkin disease." Blood 99, no. 2 (January 15, 2002): 690–93. http://dx.doi.org/10.1182/blood.v99.2.690.

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Abstract The HLA region has long been implicated in sporadic and familial Hodgkin disease (HD), with recent case-control studies suggesting that HLA class II loci predispose to sporadic nodular sclerosis HD (NSHD). To determine whether this predisposition extends to familial HD, HLA class II loci (DRB1, DQA1, DQB1, DRB3, DRB4, and DRB5) and transporter associated with antigen processing (TAP) loci (TAP1, TAP2) were investigated in 100 members of 16 families with at least 2 confirmed cases of HD. With the use of the transmission disequilibrium test, evidence for linkage disequilibrium with familial HD and, in particular, familial NSHD was obtained for the DRB1*1501-DQA1*0102-DQB1*0602 haplotype, the TAP1 allele encoding Ile at residue 333, and the DRB5-0101 allele. These 3 markers were in linkage disequilibrium and may not represent independent susceptibility regions. Use of a family-based approach excludes population stratification as an explanation for these findings.

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28

Queiro, Rubén, Patricia Tejón, Sara Alonso, Pablo Coto, Carlos López-Larrea, Jesús Martínez-Borra, and Segundo González. "The Region Centromeric to HLA-C Is a Key Region for Understanding the Phenotypic Variability of Psoriatic Arthritis." ISRN Dermatology 2014 (January 30, 2014): 1–5. http://dx.doi.org/10.1155/2014/570178.

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With the aim of clarifying the role of several polymorphisms around the HLA-C locus in the clinical expression of PsA, the distribution of several polymorphic markers and genes located around the HLA-C locus was analyzed in a well-established cohort of 110 patients with PsA, 50 patients with psoriasis alone, and 110 healthy controls. The frequency of these genes was also analyzed by PsA articular models, based on three main subgroups: oligoarthritis, polyarthritis, and spondylitis. Distal interphalangeal joint (DIP) involvement was associated with the presence of MICB-CA20 (OR 6.0, 95% CI: 1.58–22.69, P=0.005). HLA-DRB*07 was associated with oligoarticular forms of PsA (OR 4.1, 95% CI: 1.8–9.3, P=0.0007). The spondylitic forms overexpressed the antigen HLA-B*27 (OR 5.7, 95% CI: 2.4–13.6, P=0.0001). MICA-A5.1 showed association with polyarthritis (OR 3.7, 95% CI: 1.5–8.8, P=0.006). Genes telomeric to HLA-C were overexpressed in psoriasis but not in PsA subphenotypes. This study shows that the region centromeric to HLA-C is a key region that expresses not only disease risk genes but also genes that help explain the phenotypic variability of PsA.

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29

Yoon, Taejin, Henriette Macmillan, Sujin Roh, and Elizabeth Mellins. "Transmembrane domain interaction regulates HLA-DO inhibition of HLA-DM (100.20)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 100.20. http://dx.doi.org/10.4049/jimmunol.186.supp.100.20.

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Abstract Peptide-loading of MHC class II (e.g. HLA-DR) is regulated by the peptide exchange catalyst, HLA-DM (DM). HLA-DO (DO) inhibits DM, but the mechanism is not established. We found that a DMB point mutant with aberrant glycosylation at DMβ108 failed to co-precipitate with DR3 at pH 5, but was able to bind DO at this pH, and conversely, precipitated with DR3, but not with DO, at pH 7. Additional mutants implicated a unique region of DMβ in DO binding, distinct from but near the putative DR interface in human B cell line. However, FRET assay results with soluble recombinant proteins are inconsistent with these observations and argue that DO binds to a surface overlapping with the DR binding surface on DM. These contradictory results suggested that the transmembrane (TM) regions influence the interaction between DM and DO. We found that TM regions of DM and DO contain not only αβ dimerization motifs, but also intermolecular interaction motifs. A DM TM mutant with reduced DO interaction showed increased DM function in cells, suggesting that TM interaction between DM and DO regulates DO inhibition of DM. Taken together our results suggest DO inhibition is noncompetitive in cells and are consistent with previous evidence for a trimolecular complex (DR/DM/DO) in a B cell line.

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30

Okoye, R. C., W. Ollier, D. Jaraquemada, J. Awad, C. Navarrete, S. Cutbush, D. Carthy, A. Dos-Santos, and H. Fstenstein. "HLA-D region heterogeneity in a Nigerian population." Tissue Antigens 33, no. 4 (April 1989): 445–56. http://dx.doi.org/10.1111/j.1399-0039.1989.tb01693.x.

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31

Raymond, C. K. "Ancient haplotypes of the HLA Class II region." Genome Research 15, no. 9 (August 18, 2005): 1250–57. http://dx.doi.org/10.1101/gr.3554305.

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32

EIiaou, J. F., V. Pinet, and J. Clot. "Ddel polymorphism in the HLA-DRA regulatory region." Nucleic Acids Research 18, no. 23 (1990): 7195. http://dx.doi.org/10.1093/nar/18.23.7195.

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33

Fletcher, J., C. Mijovic, D. Jenkins, A. R. Bradwell, and A. H. Barnett. "HLA-D Region RFLPs and Type 1 Diabetes." Diabetic Medicine 5, no. 6 (September 1988): 596. http://dx.doi.org/10.1111/j.1464-5491.1988.tb01060.x.

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34

Gladman, Dafna D., Vernon T. Farewell, Fawnda Pellett, Cathy Schentag, and Proton Rahman. "HLA is a candidate region for psoriatic arthritis." Human Immunology 64, no. 9 (September 2003): 887–89. http://dx.doi.org/10.1016/s0198-8859(03)00162-9.

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35

Geraphty, Daniel E., Marta Janer, and Thierry Guillaudeux. "Genomic sequencing of the HLA class I region." Human Immunology 47, no. 1-2 (April 1996): 66. http://dx.doi.org/10.1016/0198-8859(96)85045-2.

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36

Yao, Zhu, Andrea Volgger, Siegfried Scholz, and Ekkehard D. Albert. "Sequence polymorphism in the HLA-B promoter region." Immunogenetics 41, no. 6 (April 1995): 343–53. http://dx.doi.org/10.1007/bf00163991.

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37

Guardiola, John, Antonella Maffei, Stefan Carrel, and Roberto S. Accolla. "Molecular genotyping of the HLA-DQ ? gene region." Immunogenetics 27, no. 1 (January 1988): 12–18. http://dx.doi.org/10.1007/bf00404438.

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38

Hanson, Isabel, Jiannis Ragoussis, and John Trowsdale. "Organization of the human HLA-class-II region." International Journal of Cancer 47, S6 (1991): 18–19. http://dx.doi.org/10.1002/ijc.2910470706.

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39

Foissac, A., M. Fort, J. Clayton, M. Abbal, C. Raffoux, A. Moine, J. C. Bensa, J. D. Bignon, P. Mercier, and A. Cambon-Thomsen. "Microsatellites in the HLA region: HLA prediction and strategies for bone marrow donor registries." Transplantation Proceedings 33, no. 1-2 (February 2001): 491–92. http://dx.doi.org/10.1016/s0041-1345(00)02107-2.

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40

Bennetts, Bruce H., Suzy M. Teutsch, Marc McW Buhler, Robert N. S. Heard, and Graeme J. Stewart. "HLA-DMB gene and HLA-DRA promoter region polymorphisms in Australian multiple sclerosis patients." Human Immunology 60, no. 9 (September 1999): 886–93. http://dx.doi.org/10.1016/s0198-8859(99)00054-3.

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41

Gongora, R., F. Figueroa, and J. Klein. "Complex origin of the HLA-DR10 haplotype." Journal of Immunology 159, no. 12 (December 15, 1997): 6044–51. http://dx.doi.org/10.4049/jimmunol.159.12.6044.

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Abstract The region of the HLA complex occupied by the DRB genes has undergone many rearrangements in the course of primate evolution. The rearrangements have produced a number of haplotypes differing from one another in the number and composition of the DRB genes. Some of the rearrangements also affected the DRB genes themselves. Selective intron sequencing has revealed the DR10 haplotype to be composed of at least three segments, each of different origin. The haplotype carries three DRB genes (gene fragments): DRB1*10, DRB6, and DRB9. The 5' end of the DRB1*10 gene, from the promoter region to a site in intron 1 approximately 500 bp from the beginning of exon 2, is derived from a DRB1*03-like gene. The segment of the DR10 haplotype encompassing the rest of the DRB1*10 gene and extending to the region between the DRB1 and DRB6 genes is of independent origin; it diverged from other DRB genes (DRB1*01 and DRB1*03) approximately 30 million years ago. Finally, the third segment encompassing the remainder of the DR10 haplotype is derived from a DR1-like haplotype. Since the functional part of the DR10 haplotype is of independent origin, there is little justification for the currently common practice of placing the haplotype together with DR1 in the group of DR1 haplotypes. The rearrangements in the DR haplotypes may constitute one of several mechanisms for increasing diversity at the DRB loci. The region of high instability seems to be flanked by conservatively evolving regions.

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42

Anderson, Stephen, and Hongchuan Li. "Analysis of regulatory elements in the HLA-A, HLA-B, and HLA-C genes provides insights into the specific role of each HLA in the immune system." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 59.11. http://dx.doi.org/10.4049/jimmunol.202.supp.59.11.

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Abstract We have conducted a detailed analysis of regulatory elements present in the upstream region of the HLA-A, HLA-B, and HLA-C genes. Significant differences in transcription factor-binding sites were identified in a tissue-specific promoter located 1.3 kb upstream, an enhancer element at −800 bp, and the core promoter region, that alter both the tissue specificity and expression level of the HLA genes. The upstream promoter has changed from macrophage-specificity in HLA-A to an unknown specificity in HLA-B, and it has gained NK specificity in HLA-C that is coupled with an elaborate post-transcriptional regulatory mechanism. The −800 enhancer region contains distinct arrays of transcription factor-binding sites in the HLA-A, HLA-B, and HLA-C genes. A comparison of the proximal promoter region of these three genes revealed multiple differences in key enhanceosome and cytokine-inducible elements, and the presence of additional trophoblast-specific elements in the HLA-C promoter. Furthermore, a comparison of HLA-C alleles reveals functional differences in transcription factor-binding sites that likely reflects allele-specific tuning of expression. A more complete understanding of the molecular evolution of regulatory elements between the HLA-A, HLA-B, and HLA-C genes will provide important clues with regard to the separate immunological functions of the three MHC class I genes present in humans.

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43

Veiga-Castelli, Luciana C., Cristhianna V. Collares, Iane O. Porto, Elaine Moises, Maria Cristina Foss-Freitas, Celso T. Mendes-Junior, Erick C. Castelli, and Eduardo A. Donadi. "P014 HLA-C, HLA-E and HLA-G regulatory and coding region polymorphisms in patients exhibiting gestational diabetes mellitus." Human Immunology 78 (September 2017): 64. http://dx.doi.org/10.1016/j.humimm.2017.06.074.

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44

Fakiola, Michaela, Amy Strange, Heather J. Cordell, E. Nancy Miller, Matti Pirinen, Zhan Su, Anshuman Mishra, et al. "Common variants in the HLA-DRB1–HLA-DQA1 HLA class II region are associated with susceptibility to visceral leishmaniasis." Nature Genetics 45, no. 2 (January 6, 2013): 208–13. http://dx.doi.org/10.1038/ng.2518.

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45

Liu, Yanbing, Hongbo Sun, Wenhui Fan, and Tianyuan Xiao. "A parallel matching algorithm based on order relation for HLA data distribution management." International Journal of Modeling, Simulation, and Scientific Computing 06, no. 02 (May 29, 2015): 1540002. http://dx.doi.org/10.1142/s1793962315400024.

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In distribution simulation based on High-level architecture (HLA), data distribution management (DDM) is one of HLA services for the purpose of filtering the unnecessary data transferring over the network. DDM admits the sending federates and the receiving federates to express their interest using update regions and subscription regions in a multidimensional routing space. There are several matching algorithms to obtain overlap information between the update regions and subscription regions. When the number of regions increase sharply, the matching process is time consuming. However, the existing algorithms is hard to be parallelized to take advantage of the computing capabilities of multi-core processors. To reduce the computational overhead of region matching, we propose a parallel algorithm based on order relation to accelerate the matching process. The new matching algorithm adopts divide-and-conquer approach to divide the regions into multiple region bound sublists, each of which comprises parts of region bounds. To calculate the intersection inside and amongst the region bound sublists, two matching rules are presented. This approach has good performance since it performs region matching on the sublists parallel and does not require unnecessary comparisons within regions in different sublists. Theoretical analysis has been carried out for the proposed algorithm and experimental result shows that the proposed algorithm has better performance than major existing DDM matching algorithms.

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46

Hitman, G. A., P. K. Karir, J. A. Sachs, A. Ramachandran, C. Snehalatha, M. Viswanathan, and V. Mohan. "HLA-D Region RFLPs Indicate That Susceptibility to Insulin-dependent Diabetes in South India is Located in the HLA-DQ Region." Diabetic Medicine 5, no. 1 (January 1988): 57–60. http://dx.doi.org/10.1111/j.1464-5491.1988.tb00942.x.

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47

Crowley, N. J., T. L. Darrow, M. A. Quinn-Allen, and H. F. Seigler. "MHC-restricted recognition of autologous melanoma by tumor-specific cytotoxic T cells. Evidence for restriction by a dominant HLA-A allele." Journal of Immunology 146, no. 5 (March 1, 1991): 1692–99. http://dx.doi.org/10.4049/jimmunol.146.5.1692.

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Abstract Autologous melanoma-specific CTL recognize a common tumor-associated Ag (TAA) in the context of HLA class I antigens. We have demonstrated that HLA-A2 can be a restricting Ag and, in T cell lines homozygous for HLA-A2, that CTL can be generated by stimulation with HLA-A2 allogeneic melanomas. In the current study, we have investigated T cell lines from patients who are heterozygous at HLA-A region locus, to determine the relative importance of each A-region allele in this MHC-restricted recognition of tumor. We have shown that HLA-A1 can be a restricting Ag, and that allogeneic melanomas expressing HLA-A1 can substitute for the autologous tumor in the generation of HLA-A1-restricted CTL. However, when T cell lines express both HLA-A1 and HLA-A2, the HLA-A2 allele governed restriction of the melanoma TAA. Three autologous-stimulated HLA-A1, A2 CTL lines all demonstrated restriction by the HLA-A2 allele, when examined in cytotoxicity assays, cold-competition assays, and proliferation assays. There was no evidence of restriction by the second HLA-allele, HLA-A1. Although the autologous-stimulated CTL use a single A-region allele for tumor recognition, the autologous HLA-A1, A2 tumors are lysed by both HLA-A1-restricted and HLA-A2-restricted CTL. The dominance of restricting alleles was further demonstrated when HLA-matched allogeneic melanomas were used as the stimulating tumor to generate tumor-specific CTL. Stimulation of the heterozygous (HLA-A1, A2) lymphocytes with HLA-A2-matched allogeneic melanomas resulted in CTL specific for the autologous tumor, and restricted by the HLA-A2 Ag. However, stimulation with an HLA-A1-matched allogeneic melanoma failed to induce tumor-specific CTL restricted by the HLA-A1 Ag. The data suggest there is a dominance of HLA-A region Ag at the level of the T cell, such that only one is restricting in the recognition of the autologous melanoma. At the level of the tumor, however, the TAA is expressed in the context of both HLA-A region alleles. We can generate specific CTL from lymph node cells or PBL and HLA-A region matched allogeneic melanomas; however, because most patients are heterozygous at the HLA-A region locus, an understanding of the dominant restricting alleles must be obtained so that an appropriately matched allogeneic melanoma can be selected.

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48

Mo, X. D., J. Wang, and T. Zhang. "Full-length sequencing of the HLA region identified a novel allele, HLA-B*52:70." HLA 90, no. 4 (July 20, 2017): 253–54. http://dx.doi.org/10.1111/tan.13089.

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Sterkers, G., D. Zeliszewski, A. M. Chaussee, I. Deschamps, M. P. Font, C. Freidel, J. Hors, H. Betuel, J. Dausset, and J. P. Levy. "HLA-DQ rather than HLA-DR region might be involved in dominant nonsusceptibility to diabetes." Proceedings of the National Academy of Sciences 85, no. 17 (September 1, 1988): 6473–77. http://dx.doi.org/10.1073/pnas.85.17.6473.

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Bontrop, Ronald E., Marcel G. J. Tilanus, Marlies M. A. Mikulski, Dienne G. Elferink, Annemarie Termijtelen, Rene R. P. de Vries, Jon J. van Rood, and Marius J. Giphart. "Polymorphism and complexity of HLA-DR: evidence for intra-HLA-DR region crossing-over events." Immunogenetics 27, no. 1 (January 1988): 40–45. http://dx.doi.org/10.1007/bf00404442.

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