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Статті в журналах з теми "Genomic HLA"

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Автор: Grafiati

Опубліковано: 31 травня 2023

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1

Amar, A., G. T. Nepom, E. Mickelson, H. Erlich, and J. A. Hansen. "HLA-DP and HLA-DO genes in presumptive HLA-identical siblings: structural and functional identification of allelic variation." Journal of Immunology 138, no. 6 (March 15, 1987): 1947–53. http://dx.doi.org/10.4049/jimmunol.138.6.1947.

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Abstract We analyzed HLA class II genomic polymorphisms in three families in which bone marrow transplantation was performed between individuals presumed to be HLA identical, but in which unexplained mixed lymphocyte culture reactivity was observed. These families were characterized by classical HLA serology, MLC, and DP typing. In each family, a pair of "HLA-identical" siblings demonstrated a small proliferative response in bidirectional MLC. Southern blotting analysis performed with cDNA probes for DQ alpha, DP alpha, and DP beta identified DP genomic differences in each case. Hybridization of Bgl II-digested genomic DNA with a DP alpha cDNA probe revealed three prominent polymorphic fragments (7.7, 5.8, and 3.7 kb), which discriminated between presumptive identical siblings and indicated crossover events within HLA. Similarly, hybridization of SstI-digested genomic DNA with a DP beta cDNA probe, although resulting in a more complex pattern, identified DP genomic disparity between the presumed HLA identical siblings. Hybridization of SstI-digested DNA from two families with evidence of DP recombination was performed by using an oligonucleotide probe specific for the newly described HLA class II gene DO beta. Two major polymorphic fragments, at 6.2 and 3.3 kb, segregated in these families and localized the crossovers flanking the DO beta gene between the DQ and DP loci. The contribution of the antigenic differences marked by these HLA DP and DO DNA polymorphisms to allorecognition in MLR and in graft-vs-host disease are discussed.

2

Meyer, Diogo, Vitor R. C. Aguiar, Bárbara D. Bitarello, Débora Y. C. Brandt, and Kelly Nunes. "A genomic perspective on HLA evolution." Immunogenetics 70, no. 1 (July 7, 2017): 5–27. http://dx.doi.org/10.1007/s00251-017-1017-3.

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3

Drover, Sheila, and William H. Marshall. "Transfection of HLA genes using genomic DNA." Human Immunology 31, no. 4 (August 1991): 293–98. http://dx.doi.org/10.1016/0198-8859(91)90102-f.

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4

Hansen, H. E., L. O. Vejerslev, and S. Olesen Larsen. "Hydatidiform mole and HLA. III. HLA-antigen expression related to genomic origin." Tissue Antigens 32, no. 3 (September 1988): 162–69. http://dx.doi.org/10.1111/j.1399-0039.1988.tb01653.x.

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5

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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6

Balas, A., D. Planelles, M. Rodríguez-Cebriá, N. Puig, and J. L. Vicario. "Genomic sequences of HLA-A*68:169, HLA-B*07:298 and HLA-B*39:129." International Journal of Immunogenetics 45, no. 3 (March 8, 2018): 140–42. http://dx.doi.org/10.1111/iji.12360.

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7

D'Amato, Mauro, Rosa Sorrentino, and Roberto Tosi. "Extremely simplified sample preparation for HLA genomic typing." Tissue Antigens 39, no. 1 (January 1992): 40–41. http://dx.doi.org/10.1111/j.1399-0039.1992.tb02156.x.

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8

Yamashita, T., K. Tokunaga, K. Tadokoro, T. Juji, and Y. Taketanl. "Correction of the HLA-G*01012 genomic sequence." Tissue Antigens 49, no. 6 (June 1997): 673–74. http://dx.doi.org/10.1111/j.1399-0039.1997.tb02823.x.

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9

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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10

Shiina, Takashi. "Next generation sequencing based HLA genomic and polymorphism analyses." Major Histocompatibility Complex 22, no. 2 (2015): 84–94. http://dx.doi.org/10.12667/mhc.22.84.

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11

Ramachandran, Dhanya, and Thilo Dörk. "Genomic Risk Factors for Cervical Cancer." Cancers 13, no. 20 (October 13, 2021): 5137. http://dx.doi.org/10.3390/cancers13205137.

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Cervical cancer is the fourth common cancer amongst women worldwide. Infection by high-risk human papilloma virus is necessary in most cases, but not sufficient to develop invasive cervical cancer. Despite a predicted genetic heritability in the range of other gynaecological cancers, only few genomic susceptibility loci have been identified thus far. Various case-control association studies have found corroborative evidence for several independent risk variants at the 6p21.3 locus (HLA), while many reports of associations with variants outside the HLA region remain to be validated in other cohorts. Here, we review cervical cancer susceptibility variants arising from recent genome-wide association studies and meta-analysis in large cohorts and propose 2q14 (PAX8), 17q12 (GSDMB), and 5p15.33 (CLPTM1L) as consistently replicated non-HLA cervical cancer susceptibility loci. We further discuss the available evidence for these loci, knowledge gaps, future perspectives, and the potential impact of these findings on precision medicine strategies to combat cervical cancer.

12

Balas, A., F. García-Sánchez, R. Alenda, and J. L. Vicario. "Genomic sequences of two novel HLA-C alleles, HLA-C*15:143 and HLA-C*07:109:02." HLA 90, no. 6 (September 7, 2017): 374–76. http://dx.doi.org/10.1111/tan.13137.

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13

Dapprich, Johannes, Valerie McCarro, Cynthia Turino, Genaro Scavello, and Nancy Murphy. "Multiplexed haploseparation of genomic DNA for HLA-A, HLA-B and HLA-DRB1 by haplotype-specific extraction (HSE)." Human Immunology 66, no. 8 (August 2005): 69. http://dx.doi.org/10.1016/j.humimm.2005.08.131.

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14

Bainbridge, David R. J., Shirley A. Ellis, and Ian L. Sargent. "Little Evidence of HLA-G mRNA Polymorphism in Caucasian or Afro-Caribbean Populations." Journal of Immunology 163, no. 4 (August 15, 1999): 2023–27. http://dx.doi.org/10.4049/jimmunol.163.4.2023.

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Abstract HLA-G is a nonclassical class I MHC molecule of unknown function expressed on human trophoblast. The level of polymorphism at the HLA-G locus is of considerable importance, since the paternally inherited gene product is exposed to the maternal immune system during pregnancy. However, previous studies of HLA-G polymorphism using genomic DNA samples have produced conflicting results. Our aim was to investigate polymorphism in trophoblast HLA-G mRNA from pregnancies in ten Caucasian and twelve Afro-Caribbean women by RT-PCR. A similar PCR protocol was also applied to umbilical cord blood genomic DNA from two Caucasian and two Afro-Caribbean neonates. Caucasian cDNA yielded only two different sequences: G*01011, and one containing a previously reported synonymous substitution. Afro-Caribbean samples yielded these sequences as well as one previously reported conservative (leucine-to-isoleucine) substitution. PCR amplification from genomic DNA samples from both populations using previously published primer pairs generated sequences containing multiple substitutions, many of which were nonsynonymous. More than two sequences were produced from genomic DNA from each individual. In contrast, amplification from the same genomic DNA using new primers complementary to exons of the HLA-G gene yielded the same few sequences generated from cDNA. These results suggest that polymorphism at the HLA-G locus is extremely limited in Caucasian and Afro-Caribbean populations. This suggests that spurious polymorphism has been reported in African Americans due to the use of intron-complementary PCR primers on genomic DNA samples. The monomorphic nature of HLA-G may allow trophoblast to carry out the immunological functions of class I-bearing tissues without compromising successful pregnancy.

15

Zarling, Angela L., Kelly D. Smith, Charles T. Lutz, and D. R. Lee. "Correction of the HLA-Cw3 genomic sequence tentatively identifies it as HLA-Cw * 0304." Immunogenetics 44, no. 1 (April 29, 1996): 82–83. http://dx.doi.org/10.1007/s002510050093.

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16

Vadva, Larsen, Propp, Trautwein, Alford, and Alper. "A New Pedigree-Based SNP Haplotype Method for Genomic Polymorphism and Genetic Studies." Cells 8, no. 8 (August 5, 2019): 835. http://dx.doi.org/10.3390/cells8080835.

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Single nucleotide polymorphisms (SNPs) are usually the most frequent genomic variants. Directly pedigree-phased multi-SNP haplotypes provide a more accurate view of polymorphic population genomic structure than individual SNPs. The former are, therefore, more useful in genetic correlation with subject phenotype. We describe a new pedigree-based methodology for generating non-ambiguous SNP haplotypes for genetic study. SNP data for haplotype analysis were extracted from a larger Type 1 Diabetes Genetics Consortium SNP dataset based on minor allele frequency variation and redundancy, coverage rate (the frequency of phased haplotypes in which each SNP is defined) and genomic location. Redundant SNPs were eliminated, overall haplotype polymorphism was optimized and the number of undefined haplotypes was minimized. These edited SNP haplotypes from a region containing HLA-DRB1 (DR) and HLA-DQB1 (DQ) both correlated well with HLA-typed DR,DQ haplotypes and differentiated HLA-DR,DQ fragments shared by three pairs of previously identified megabase-length conserved extended haplotypes. In a pedigree-based genetic association assay for type 1 diabetes, edited SNP haplotypes and HLA-typed HLA-DR,DQ haplotypes from the same families generated essentially identical qualitative and quantitative results. Therefore, this edited SNP haplotype method is useful for both genomic polymorphic architecture and genetic association evaluation using SNP markers with diverse minor allele frequencies.

17

Leventhal, Joseph R., James M. Mathew, Daniel R. Salomon, Sunil M. Kurian, Manikkam Suthanthiran, Anat Tambur, John Friedewald, et al. "Genomic Biomarkers Correlate with HLA-Identical Renal Transplant Tolerance." Journal of the American Society of Nephrology 24, no. 9 (June 20, 2013): 1376–85. http://dx.doi.org/10.1681/asn.2013010068.

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18

Steinle, Alexander, Elfriede NiEner, and Dolores J. Schendel. "Isolation and characterization of a genomic HLA-Cw6 clone." Tissue Antigens 39, no. 3 (March 1992): 134–37. http://dx.doi.org/10.1111/j.1399-0039.1992.tb01923.x.

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19

Papassavas, E., J. Stephanoyannis, M. Papadimitropoulos, E. Stamathioudaki, G. Vrioni, M. Spyropoulou-Vlachou, and C. Stavropoulos-Giokas. "Genomic HLA class I typing by using ARMS/PCR." Human Immunology 47, no. 1-2 (April 1996): 45. http://dx.doi.org/10.1016/0198-8859(96)84922-6.

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20

Takeuchi, Yumiko, Kazumasa Matsuki, Yoshimi Saito, Tsuneaki Sugimoto, and Takeo Juji. "HLA-D Region Genomic Polymorphism Associated with Takayasu's Arteritis." Angiology 41, no. 6 (June 1990): 421–26. http://dx.doi.org/10.1177/000331979004100601.

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21

Shaman, Jeffrey, Emily von Scheven, Philip Morris, Ming-der Y. Chang, and Elizabeth Mellins. "Analysis of HLA-DMB mutants and -DMB genomic structure." Immunogenetics 41, no. 2-3 (January 1995): 117–24. http://dx.doi.org/10.1007/bf00182322.

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22

Pyke, Rachel, Steven Dea, Dattatreya Mellacheruvu, Charles Abbott, Simo Zhang, Lee McDaniel, Eric Levy, et al. "79 Extensively validated HLA LOH algorithm demonstrates an association between HLA LOH and genomic instability." Journal for ImmunoTherapy of Cancer 9, Suppl 2 (November 2021): A88. http://dx.doi.org/10.1136/jitc-2021-sitc2021.079.

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BackgroundHuman Leukocyte Antigen (HLA) genes are critical for the presentation of neoantigens to the immune system by cancer cells. Deletion of HLA alleles, known as HLA loss of heterozygosity (LOH), has been highlighted as a key immune escape mechanism. Validated algorithms to detect HLA LOH from sequencing data are critical for exploring the biological impact of HLA LOH and assessing its utility as a clinical biomarker.MethodsWe developed DASH (Deletion of Allele-Specific HLAs), a machine learning algorithm trained on data from 279 patients on the ImmunoID NeXT Platform using features that account for probe capture variability between alleles and incorporate information from the regions flanking each HLA gene. To understand the contribution of boosted sequencing in the HLA region of the ImmunoID NeXT Platform, we performed an in silico downsampling analysis. To assess DASH’s performance at variable tumor purities and HLA LOH subclonalities we identified three tumor-normal cell lines with HLA LOH and created in silico mixtures. Furthermore, after designing patient-specific primers for 21 patients that target specific alleles, we applied digital PCR (dPCR) to validate the HLA allele copy number status of the patients. Finally, we applied DASH to 611 patients spanning 15 tumor types.ResultsIn cross validation analyses across patient samples, DASH achieved 98.7% specificity and 92.9% sensitivity while LOHHLA, a widely used algorithm, only reached 94.3% and 78.8%, respectively (figure 1). Downsampling analyses demonstrated that DASH benefits significantly from the boosted HLA sequencing on the ImmunoID NeXT Platform, dropping 0.06 in F-score after downsampling to the sequencing depth of other exome platforms. In cell line mixture analyses, DASH demonstrates greater than 99% specificity across all tumor purity and sub-clonality levels and greater than 98% sensitivity for above 27% tumor purity. Moreover, DASH demonstrated 100% sensitivity and specificity in dPCR experiments across 21 tumor samples with stable controls. We applied DASH to a large pan-cancer cohort and found that 18% of patients had HLA LOH (figure 2). We identified strong associations between HLA LOH and genomic instability. Moreover, we demonstrated relationships between HLA LOH and markers of immune pressure, such as a correlation with CD274 (PD-1) expression and allele-specific neoantigen enrichment for deleted HLA alleles.ConclusionsDASH, a highly sensitive HLA LOH algorithm that has been extensively validated using cross validation, in silico downsampling, cell line mixtures and dPCR, has demonstrated the widespread impact of HLA LOH in a large pan-cancer cohort.Abstract 79 Figure 1Bar plots showing the sensitivity and specificities scores across ImmunoID NeXT cross validation samples between LOHHLA (blue) and DASH (green).Abstract 79 Figure 2Bar plots denoting the number of patients and the frequency of HLA LOH in each tumor type cohort. 95% confidence intervals are shown with the thin dark grey bars. Only cohorts with at least 10 patients are shown

23

MURTHY, Prerana Madhusudhana, Anupama Cheleri NEDUVAT, Cheemalamarri VEENADHAR, Sudarson SUNDARRAJAN, and Sriram PADMANABHAN. "Human Saliva and Dried Saliva Spots as Source of DNA for PCR based HLA Typing using a Combination of Taq DNA Polymerase and AccuPrimeTaq Polymerase." Walailak Journal of Science and Technology (WJST) 17, no. 2 (February 28, 2019): 113–27. http://dx.doi.org/10.48048/wjst.2020.4430.

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Genomic DNA extracted from human saliva samples showed high inter-subject variations in DNA yield, compelling the need to explore a methodology for the accurate quantitation of the extracted genomic DNA. Quantitative assessment of DNA extracted from saliva was achieved using human coagulation factor XIII as an internal control for subsequent downstream applications of amplification of human leucocyte antigen (HLA) genes by PCR. The PCR signals for the HLA target genes, namely, HLA-A, -B, -C , DPB1, DQB1, and DRB1 of exons 2 and 3, improved greatly with the use of a combination of Taq DNA polymerase and AccuPrimeTaq DNA polymerase. We also describe a new method of using dried saliva spots (DSS) as an alternate source of genomic DNA for HLA typing. PCR-based typing of DNA from human saliva offers a potential method for HLA typing and amplification, and typing of DNA, thus presented, could be applied in forensic science to saliva samples recovered from crime scenes.

24

Zhang, Kun-Lian, Xiao-Feng Li, Xu Zhang, Feng-Qiu Lin, and Jian-Ping Li. "The novel HLA-B allele, HLA -B*50:31 , was identified by sequencing genomic DNA." HLA 92, no. 6 (October 29, 2018): 415–17. http://dx.doi.org/10.1111/tan.13391.

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25

Li, J. P., X. F. Li, X. Zhang, F. Q. Lin, and K. L. Zhang. "The novel HLA-B allele,HLA-B*07:110, was identified by sequencing genomic DNA." Tissue Antigens 82, no. 6 (October 24, 2013): 432–33. http://dx.doi.org/10.1111/tan.12222.

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26

Yelavarthi, K. K., C. M. Schmidt, R. G. Ehlenfeldt, H. T. Orr, and J. S. Hunt. "Cellular distribution of HLA-G mRNA in transgenic mouse placentas." Journal of Immunology 151, no. 7 (October 1, 1993): 3638–45. http://dx.doi.org/10.4049/jimmunol.151.7.3638.

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Abstract The human MHC class I gene, HLA-G, is unique among members of the class I gene family in that it is nonpolymorphic, and expression is primarily restricted to extraembryonic tissues. To examine regulatory elements that direct tissue- and cell lineage-specific expression of this gene, transgenic mice expressing HLA-G have been established. In this study, in situ hybridization was used to evaluate the cellular distribution of HLA-G mRNA in transgenic placentas. Extraembryonic tissues were obtained at gestation day 12.5 from embryos that had been microinjected with either 6.0 or 5.7 kb of HLA-G genomic DNA and had been transferred into pseudopregnant HLA-G transgenic mice or Swiss mice. The 6.0 kb transgene contained an additional 250 bp at the extreme 5'-end of the upstream region. Genotype of the recipient had no discernable effect on the cellular distribution of HLA-G mRNA. HLA-G mRNA was present in both trophoblast and mesenchymal cells in transgenic placentas carrying 6.0 kb of genomic HLA-G, a pattern strikingly similar to that of HLA-G message distribution in early gestation human placentas. By contrast, in placentas from embryos carrying 5.7 kb HLA-G DNA, specific mRNA was found primarily in mesenchymal cells at the base of the placenta. Thus, the 6.0 genomic fragment contains elements capable of directing HLA-G expression in placentas, and is particularly influential in the trophoblastic cell lineage.

27

Heinold, A., E. Schaller-Suefling, G. Opelz, S. Scherer, and T. H. Tran. "Identification of two novel HLA alleles, HLA-A*02010103 and HLA-B*4455, and characterization of the complete genomic sequence of HLA-A*290201." Tissue Antigens 72, no. 4 (October 2008): 397–400. http://dx.doi.org/10.1111/j.1399-0039.2008.01100.x.

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28

Fumet, Jean-David, Emilie Lardenois, Isabelle Ray-Coquard, Philipp Harter, Florence Joly, Ulrich Canzler, Caroline Truntzer, et al. "Genomic Instability Is Defined by Specific Tumor Microenvironment in Ovarian Cancer: A Subgroup Analysis of AGO OVAR 12 Trial." Cancers 14, no. 5 (February 25, 2022): 1189. http://dx.doi.org/10.3390/cancers14051189.

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Background: Following disappointing results with PD-1/PD-L1 inhibitors in ovarian cancer, it is essential to explore other immune targets. The aim of this study is to describe the tumor immune microenvironment (TME) according to genomic instability in high grade serous ovarian carcinoma (HGSOC) patients receiving primary debulking surgery followed by carboplatin-paclitaxel chemotherapy +/− nintedanib. Methods: 103 HGSOC patients’ tumor samples from phase III AGO-OVAR-12 were analyzed. A comprehensive analysis of the TME was performed by immunohistochemistry on tissue microarray. Comparative genomic hybridization was carried out to evaluate genomic instability signatures through homologous recombination deficiency (HRD) score, genomic index, and somatic copy number alterations. The relationship between genomic instability and TME was explored. Results: Patients with high intratumoral CD3+ T lymphocytes had longer progression-free survival (32 vs. 19.6 months, p = 0.009) and overall survival (OS) (median not reached). High HLA-E expression on tumor cells was associated with a longer OS (median OS not reached vs. 52.9 months, p = 0.002). HRD profile was associated with high HLA-E expression on tumor cells and an improved OS. In the multivariate analysis, residual tumor, intratumoral CD3, and HLA-E on tumor cells were more predictive than other parameters. Conclusions: Our results suggest HLA-E/CD94-NKG2A/2C is a potential immune target particularly in the HRD positive ovarian carcinoma subgroup.

29

Curcio, M., S. Presciuttini, R. Sciarrino, S. Fornaciari, M. L. Mariotti, and F. Scatena. "Identification and characterization of a novel HLA-A allele, HLA-A*68:105, by genomic sequencing." International Journal of Immunogenetics 41, no. 6 (October 15, 2014): 484–85. http://dx.doi.org/10.1111/iji.12153.

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30

Leventhal, J. R., J. M. Mathew, D. R. Salomon, S. M. Kurian, J. J. Friedewald, L. Gallon, I. Konieczna, et al. "Nonchimeric HLA‐Identical Renal Transplant Tolerance: Regulatory Immunophenotypic/Genomic Biomarkers." American Journal of Transplantation 16, no. 1 (July 30, 2015): 221–34. http://dx.doi.org/10.1111/ajt.13416.

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31

Shiina, Takashi, Kazuyoshi Hosomichi, Hidetoshi Inoko, and Jerzy K. Kulski. "The HLA genomic loci map: expression, interaction, diversity and disease." Journal of Human Genetics 54, no. 1 (January 2009): 15–39. http://dx.doi.org/10.1038/jhg.2008.5.

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32

BRUSERUD, O., G. PAULSEN, G. MARKUSSEN, K. LUNDIN, A. B. THORESEN, and E. THORSBY. "Genomic HLA-DQbeta Polymorphism Associated with Insulin-Dependent Diabetes Mellitus." Scandinavian Journal of Immunology 25, no. 3 (March 1987): 235–43. http://dx.doi.org/10.1111/j.1365-3083.1987.tb01069.x.

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33

Leon, V. J., A. Garcia, and J. J. Fernandez. "Whole genomic amplification applied to low resolution typing of HLA." Human Immunology 64, no. 10 (October 2003): S82. http://dx.doi.org/10.1016/j.humimm.2003.08.150.

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34

Garziera, Marica, Lucia Scarabel, and Giuseppe Toffoli. "Hypoxic Modulation of HLA-G Expression through the Metabolic Sensor HIF-1 in Human Cancer Cells." Journal of Immunology Research 2017 (2017): 1–13. http://dx.doi.org/10.1155/2017/4587520.

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The human leukocyte antigen-G (HLA-G) is considered an immune checkpoint molecule involved in tumor immune evasion. Hypoxia and the metabolic sensor hypoxia-inducible factor 1 (HIF-1) are hallmarks of metastasization, angiogenesis, and intense tumor metabolic activity. The purpose of this review was to examine original in vitro studies carried out in human cancer cell lines, which reported data about HLA-G expression and HIF-1 mediated-HLA-G expression in response to hypoxia. The impact of HLA-G genomic variability on the hypoxia responsive elements (HREs) specific for HIF-1 binding was also discussed. Under hypoxia, HLA-G-negative cell lines might transcribe HLA-G without translation of the protein while in contrast, HLA-G-positive cell lines, showed a reduced HLA-G transcriptional activity and protein level. HIF-1 modulation of HLA-G expression induced by hypoxia was demonstrated in different cell lines. HLA-G SNPs rs1632947 and rs41551813 located in distinct HREs demonstrated a prominent role of HIF-1 binding by DNA looping. Our research revealed a fine regulation of HLA-G in hypoxic conditions through HIF-1, depending on the cellular type and HLA-G genomic variability. Specifically, SNPs found in HREs should be considered in future investigations as markers with potential clinical value especially in metastatic malignancies.

35

Pyo, Chul-Woo, Luke M. Williams, Yuki Moore, Hironobu Hyodo, Shuying Sue Li, Lue Ping Zhao, Noriko Sageshima, Akiko Ishitani, and Daniel E. Geraghty. "HLA-E, HLA-F, and HLA-G polymorphism: genomic sequence defines haplotype structure and variation spanning the nonclassical class I genes." Immunogenetics 58, no. 4 (March 29, 2006): 241–51. http://dx.doi.org/10.1007/s00251-005-0076-z.

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36

Zhu, F., Y. He, W. Zhang, J. He, J. He, X. Xu, H. Lv, and L. Yan. "Analysis for complete genomic sequence of HLA-B and HLA-C alleles in the Chinese Han population." International Journal of Immunogenetics 38, no. 4 (May 17, 2011): 281–84. http://dx.doi.org/10.1111/j.1744-313x.2011.01016.x.

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37

Santos, S., J. L. Arroyo, C. Eguizabal, A. Balas, and J. L. Vicario. "Genomic full-length sequence of two new HLA-C alleles,HLA-C*04:239andHLA-C*05:137." HLA 88, no. 6 (October 26, 2016): 313–14. http://dx.doi.org/10.1111/tan.12920.

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38

Nepom, B. S., J. Palmer, S. J. Kim, J. A. Hansen, S. L. Holbeck, and G. T. Nepom. "Specific genomic markers for the HLA-DQ subregion discriminate between DR4+ insulin-dependent diabetes mellitus and DR4+ seropositive juvenile rheumatoid arthritis." Journal of Experimental Medicine 164, no. 1 (July 1, 1986): 345–50. http://dx.doi.org/10.1084/jem.164.1.345.

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HLA-DR4, Dw4-associated haplotypes associated with IDDM and JRA were compared using genomic DNA restriction fragment analysis to distinguish among DQ beta and alpha alleles linked to DR4. DQ beta polymorphisms that subdivide the HLA-DQw3 specificity into DQ3.1 and 3.2 alleles were identified. More than 90% of DR4+ IDDM patients express one of these alleles, DQ3.2; restriction enzyme mapping indicates that the presence of this allele also accounts for the genomic fragment patterns previously reported in IDDM. Furthermore, haplo-identical siblings of DQ3.2 IDDM patients also carry the DQ3.2 allele, regardless of clinical presentation. In contrast, DR4+ JRA patients show no allelic preference at DQ beta, implicating different HLA genetic contributions in these two DR4-associated diseases.

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Inoko, H., A. Ando, M. Kimura, and K. Tsuji. "Isolation and characterization of the cDNA clone and genomic clones of a new HLA class II antigen heavy chain, DO alpha." Journal of Immunology 135, no. 3 (September 1, 1985): 2156–59. http://dx.doi.org/10.4049/jimmunol.135.3.2156.

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Abstract From a human cDNA library constructed from a consanguineous HLA-homozygous cell line, AKIBA (HLA-A24, Bw52, DR2, Dw12, DQw1, and Cp63) (Cp63, a new SB type), a cDNA clone encoding a new HLA class II antigen heavy chain named DQ alpha was isolated, and was analyzed by Southern blot hybridization and by nucleotide sequence determination. The nucleotide sequence of the DO alpha cDNA was distinct from those of the DR alpha, the DQ alpha, and the DP alpha cDNA, but showed some characteristic features of the class II antigen alpha-chains. We also isolated and identified genomic clones specifying the DO alpha gene. Genomic analyses of cell lines with different HLA-DR serotypes with the use of the DO alpha cDNA as a probe indicated the existence of a single DO alpha gene that exhibited little restriction enzyme polymorphism.

40

Koller, B. H., F. E. Ward, R. DeMars, and H. T. Orr. "Comparison of multiple HLA-A alleles at the DNA level by using Southern blotting and HLA-A-specific probes." Journal of Immunology 135, no. 6 (December 1, 1985): 4229–34. http://dx.doi.org/10.4049/jimmunol.135.6.4229.

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Abstract Numerous alleles of the HLA-A gene have been serologically identified. In this report we present a rapid and straightforward means to assess HLA-A polymorphism at the genomic level. Using 5' and 3' HLA-A-specific DNA probes and Southern blotting, we have placed the recognition sequences for five endonucleases relative to the coding regions of 15 HLA-A alleles. These data permit two interesting conclusions: four of the HLA-A alleles studied are associated with unique restriction fragments, and HLA-A alleles of a cross-reactive group are more closely related at the DNA level than are noncross-reactive alleles.

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Zhou, Yi-Fan, Yi Xiao, Xi Jin, Gen-Hong Di, Yi-Zhou Jiang, and Zhi-Ming Shao. "Integrated analysis reveals prognostic value of HLA-I LOH in triple-negative breast cancer." Journal for ImmunoTherapy of Cancer 9, no. 10 (October 2021): e003371. http://dx.doi.org/10.1136/jitc-2021-003371.

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BackgroundTriple-negative breast cancers (TNBCs), especially those non-immune-inflamed tumors, have a poor prognosis and limited therapies. Human leukocyte antigen (HLA)-I not only contributes to antitumor immune response and the phenotype of the tumor microenvironment, but also is a negative predictor of outcomes after immunotherapy. However, the importance of HLA functional status in TNBCs remains poorly understood.MethodsUsing the largest original multiomics datasets on TNBCs, we systematically characterized the HLA-Ⅰ status of TNBCs from the perspective of HLA-Ⅰ homogeneity and loss of heterozygosity (LOH). The prognostic significance of HLA-I status was measured. To explain the potential mechanism of prognostic value in HLA-Ⅰ status, the mutational signature, copy number alteration, neoantigen and intratumoral heterogeneity were measured. Furthermore, the correlation between HLA-Ⅰ functional status and the tumor immune microenvironment was analyzed.ResultsLOH and homogeneity in HLA-I accounted for 18% and 21% of TNBCs, respectively. HLA-I LOH instead of HLA-I homogeneity was an independent prognostic biomarker in TNBCs. In particular, for patients with non-immune-inflamed tumors, HLA-I LOH indicated a worse prognosis than HLA-I non-LOH. Furthermore, integrated genomic and transcriptomic analysis showed that HLA-I LOH was accompanied by upregulated scores of mutational signature 3 and homologous recombination deficiency scores, which implied the failure of DNA double-strand break repair. Moreover, HLA-I LOH had higher mutation and neoantigen loads and more subclones than HLA-I non-LOH. These results indicated that although HLA-I LOH tumors with failure of DNA double-strand break repair were prone to produce neoantigens, their limited capacity for antigen presentation finally contributed to poor immune selection pressure.ConclusionOur study illustrates the genomic landscape of HLA-I functional status and stresses the prognostic significance of HLA-I LOH in TNBCs. For “cold” tumors in TNBCs, HLA-I LOH indicated a worse prognosis than HLA-I non-LOH.

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Coppin, H. L., and H. O. McDevitt. "Absence of polymorphism between HLA-B27 genomic exon sequences isolated from normal donors and ankylosing spondylitis patients." Journal of Immunology 137, no. 7 (October 1, 1986): 2168–72. http://dx.doi.org/10.4049/jimmunol.137.7.2168.

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Abstract Ninety percent of individuals with ankylosing spondylitis (AS) express HLA-B27. To determine if HLA-B27 coding sequences from normal vs AS individuals show differences that might relate to the etiology of the disease, the gene coding for this allele was cloned from three different partial genomic libraries. These libraries were made with DNA from three different cell lines expressing HLA-B27: MRWC (HLA-B27, 14), obtained from an AS patient; KCA (HLA-B27, w44), obtained from a known normal individual; and MVL (HLA-B27, 27), a homozygous consanguineous cell line of unknown origin. To increase the number of clones coding for the HLA-B locus, partial libraries were made using a complete Eco RI digestion of genomic DNA in the lambda vector 607. The libraries were screened with two probes; one probe hybridizes to all HLA-A, B, C class I genes, and the other to a small subpopulation of class I genes, including the B locus. DNA from clones hybridizing with both probes was transfected into murine L cells. Cell surface expression of HLA-B27 on murine L cells was detected with a polymorphic monoclonal antibody (ME1) specific for HLA-B27, 7, 22. DNA from those clones positive for HLA-B27 by transfection was subcloned into the Xba I site of M13mp18 and the DNA sequence for exons 2 through 4 (encoding domains alpha 1, alpha 2, and alpha 3) was determined by the dideoxy technique by using synthetic oligonucleotide primers or the M13 primer. The resulting sequences show no difference between HLA-B27 alpha 1, alpha 2, alpha 3 domains from a known AS patient and a known normal individual.

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Kilpatrick, David C. "Simplified preparation from anti-coagulated blood for HLA-DR genomic typing." Tissue Antigens 41, no. 4 (April 1993): 219–20. http://dx.doi.org/10.1111/j.1399-0039.1993.tb02008.x.

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44

Tijssen, H. J., S. W. Driessen, K. P. van Houwelingen, W. A. Allebes, and I. Joosten. "Complete genomic sequence of a novel HLA-B allele, B*4456N." Tissue Antigens 73, no. 6 (June 2009): 607–9. http://dx.doi.org/10.1111/j.1399-0039.2009.01239.x.

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45

Pitchappan, R. M., V. J. Kavitha, and M. Jayalakshmi. "HLA Genomic Diversity of India and its Implications in HIV Pandemic." International Journal of Human Genetics 8, no. 1-2 (March 2008): 143–53. http://dx.doi.org/10.1080/09723757.2008.11886026.

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46

Kumar, Neeraj, Gurvinder Kaur, Nikhil Tandon, Uma Kanga, and Narinder K. Mehra. "Genomic evaluation of HLA-DR3+haplotypes associated with type 1 diabetes." Annals of the New York Academy of Sciences 1283, no. 1 (February 6, 2013): 91–96. http://dx.doi.org/10.1111/nyas.12019.

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47

Schirle, Markus. "Identification of Tumor-Associated HLA-Ligands in the Post-Genomic Era." Journal of Hematotherapy & Stem Cell Research 11, no. 6 (December 2002): 873–81. http://dx.doi.org/10.1089/152581602321080538.

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48

Leelayuwat, Chanvit, LawrenceJ Abraham, Hyacinth Tabarias, FrankT Christiansen, and RogerL Dawkins. "Genomic organization of a polymorphic duplicated region centromeric of HLA-B." Immunogenetics 36, no. 4 (July 1992): 208–12. http://dx.doi.org/10.1007/bf00215049.

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49

Leelayuwat, C., M. Pinelli, and R. L. Dawkins. "Clustering of diverse replicated sequences in the MHC. Evidence for en bloc duplication." Journal of Immunology 155, no. 2 (July 15, 1995): 692–98. http://dx.doi.org/10.4049/jimmunol.155.2.692.

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Abstract The MHC contains clusters of polymorphic duplicated genes and gene sequences. It has been thought that these duplicated genes and sequences have arisen from single gene duplications. We compared the cloned region between TNF and HLA-B with the region in close proximity to HLA-A using sequence analysis and DNA hybridization. The results indicate that several sequences existing in the region centromeric of HLA-B are also present in close proximity to HLA-A. These include sequences belonging to the P5, BAT1, and PERB11 gene families as well as HLA class I gene sequences. Interestingly, when the two regions of approximately 200 kilobases are compared, the replicated sequences are organized similarly but in an inverted fashion suggesting the existence of an historical inverted en bloc duplication. Thus, we propose that the origin of these MHC gene clusters involves several mechanisms. In addition to single gene replication, a long-range duplication of a genomic block must have occurred. It is possible that a block at the telomeric end of the MHC represents a basic functional genomic unit conserved and duplicated en bloc.

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Crinklaw, Austin, Swapnil Mahajan, Mikhail Pomaznoy, Alessandro Sette, Pandurangan Vijayanand, and Bjoern Peters. "Improving expression estimates of HLA alleles in NGS data using personalized genomic sequences and its effect on eQTL mapping." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 131.27. http://dx.doi.org/10.4049/jimmunol.202.supp.131.27.

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Abstract HLA genes are the most polymorphic in the human genome. Specific genetic variants in the HLA locus are frequently associated with diseases and other traits in GWAS studies. How much of those associations are due to functional differences in the peptide binding specificity of the various HLA genes encoded in the locus, vs. how many associations are due to differences in the expression level of the HLA genes has not been systematically determined. One hurdle in assessing HLA gene expression from RNA-Seq data when using standard analysis methods is the use of a single reference genome. We compared the estimated expression of HLA genes from 15 immune cell types of 91 individuals from the DICE database, using either the reference human genome sequence, or a personalized genome sequences based on HLA typing of the donors. This analysis showed that quantifying HLA gene expression using personalized genomic sequences allows to separate SNPs in association with HLA expression that are artifacts based on differences in read-mappability from other SNPs that are truly in association with personalized expression levels.