Journal articles: 'HLA histocompatibility antigens'

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Barbosa, J., H. Noreen, L. Emme, F. Goetz, R. Simmons, A. DeLeiva, J. Najarian, and E. J. Yunis. "Histocompatibility (HLA) Antigens and Diabetic Microangiopathy*." Tissue Antigens 7, no. 4 (December 11, 2008): 233–37. http://dx.doi.org/10.1111/j.1399-0039.1976.tb01060.x.

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Veerapathran, Anandharaman, Joseph Pidala, Francisca Beato, William E. Janssen, Xue-Zhong Yu, and Claudio Anasetti. "Tregs Specific for Minor Histocompatibility Antigens." Blood 120, no. 21 (November 16, 2012): 1891. http://dx.doi.org/10.1182/blood.v120.21.1891.1891.

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Abstract Abstract 1891 Background: The risk of acute GVHD after HSCT is increased in male recipients of female grafts. Disparities for the male-associated H-Y and other minor histocompatibility antigens (mHAs) have the capacity to sensitize alloreactive donor T cells and cause GVHD in HLA-matched recipients. These mHAs are polymorphic proteins that differ between donor and recipient and are presented as peptides by HLA molecules on recipient or donor antigen-presenting cells to donor immune cells. Currently, there is no evidence that minor histocompatibility antigen specific Tregs exist. Earlier in our laboratory, we have measured the frequency, growth requirements, and function of human blood Tregs specific for allo-MHC. In the present study, we sought to detect the frequency, expansion kinetics and characteristics of the minor antigens specific Tregs in the blood of HLA-matched sibling pair. Methods: CD4+CD25+CD127− Tregs were isolated by immunoabsorption from sibling donors, and cultured with HLA-matched sibling recipient antigen-presenting cells in the presence of IL-2, IL-15 and rapamycin. We detected 30–50 fold increase in H-TdR uptake at 6 days in Treg cultures stimulated by HLA-identical sibling compared to self DC. The precursor frequency of mHA-specific Tregs are between 7 and 43 (median - 13) cells per one million blood Tregs. The frequency of mHA-specific conventional CD4 T cells among total blood CD4 T cells is similar in HLA-matched sibling donors. Ex vivo expanded mHA-specific Tregs maintained higher levels of Foxp3 expression, retained the lymphoid homing receptor CD62L and a chemokine receptor, CCR7, suggesting that they are functional and are able to migrate to lymphoid tissue in vivo. Split well assay on day 12 demonstrated the mHA specificity, since Treg responded to restimulation with DC from the original HLA-identical sibling, but not self DC. The mHA-specific Tregs expanded to more than 100 fold in vitro, and exhibited antigen specific suppression. When Tregs were cultured at limiting dilution, we obtained 6 mHA-specific Treg clones that retained TGF-beta secretion in response to the sibling's mHA-disparate DC but not self DC. Conclusion: We demonstrated for the first time that it is possible to detect and expand mHA specific Tregs from HLA-matched sibling pairs, immunotherapy with mHA-specific Tregs may prevent GVHD. Disclosures: No relevant conflicts of interest to declare.

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Mu�oz, G., M. P. L�pez-Corell, J. F. Taboada, E. Ferrer, and M. D�az-Llopis. "Fuch's heterochromic cyclitis and HLA histocompatibility antigens." International Ophthalmology 18, no. 3 (1994): 127–30. http://dx.doi.org/10.1007/bf00915960.

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Razumova, I. Yu, A. A. Godzenko, I. A. Guseva, and O. K. Vorob’eva. "Uveitis-associated HLA class 1 histocompatibility antigens." Vestnik oftal'mologii 133, no. 5 (2017): 11. http://dx.doi.org/10.17116/oftalma2017133511-15.

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DAMGAARD-JENSEN, L., and F. KISSMEYER-NIELSEN. "HLA HISTOCOMPATIBILITY ANTIGENS IN OPEN-ANGLE GLAUCOMA." Acta Ophthalmologica 56, no. 3 (May 27, 2009): 384–88. http://dx.doi.org/10.1111/j.1755-3768.1978.tb05691.x.

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Falkenburg, J. H., H. M. Goselink, D. van der Harst, S. A. van Luxemburg-Heijs, Y. M. Kooy-Winkelaar, L. M. Faber, J. de Kroon, A. Brand, W. E. Fibbe, and R. Willemze. "Growth inhibition of clonogenic leukemic precursor cells by minor histocompatibility antigen-specific cytotoxic T lymphocytes." Journal of Experimental Medicine 174, no. 1 (July 1, 1991): 27–33. http://dx.doi.org/10.1084/jem.174.1.27.

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Minor histocompatibility (mH) antigens appear to play a major role in bone marrow transplantation (BMT) using HLA-identical donors. Previously, we reported the isolation of major histocompatibility complex (MHC)-restricted mH antigen-specific cytotoxic T lymphocytes (CTL) from patients with graft-vs.-host disease or rejection after HLA-identical BMT. We have demonstrated that mH antigens can be recognized on hematopoietic progenitor cells, and residual recipient CTL specific for mH antigens expressed on donor hematopoietic progenitor cells may be responsible for graft rejection in spite of intensive conditioning regimens in HLA-identical BMT. Here, we investigated whether mH antigen-specific CTL directed against the mH antigens HA-1 to HA-5 and the male-specific antigen H-Y were capable of antigen-specific inhibition of in vitro growth of clonogenic leukemic precursor cells. We demonstrate that mH antigen-specific CTL against all mH antigens tested can lyse freshly obtained myeloid leukemic cells, that these mH antigen-specific CTL can inhibit their clonogenic leukemic growth in vitro, and that this recognition is MHC restricted. We illustrate that leukemic (precursor) cells can escape elimination by mH antigen-specific CTL by impaired expression of the relevant MHC restriction molecule. We suggest that mH antigen-specific MHC-restricted CTL may be involved in vivo in the graft-vs.-leukemia reactivity after BMT.

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IBRAGIMOV, SH I., G. T. MANSUROVA, U. A. MAMATKULOV, and M. R. MAKHSUDOV. "Studying of relationship of Histocompatibility antigens and N-acetylation phenotype in patients of Uzbek populations with psoriasis." Vestnik dermatologii i venerologii 86, no. 1 (February 15, 2010): 67–69. http://dx.doi.org/10.25208/vdv834.

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There studied the distribution of Histocompatibility antigens and N-acetylation phenotype in patients of Uzbek populations with psoriasis and it has been revealed, that HLA antigenes A11, A28, В5, В13 and Cw3 are antigenes of predisposition to presented disease and the individuals with slow N-acetylation phenotype prevail among them. The relationship of more frequent associated Histocompatibility antigens and N-acetylation phenotype marked by the prevalence of patients with a slow phenotype in the dermatosis has been revealed in patients of Uzbek populations with psoriasis.

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Ramilyeva, I. R., Zh K. Burkitbaev, S. A. Abdrakhmanova, A. A. Turganbekova, D. K. Baimukasheva, and E. B. Zhiburt. "DISTRIBUTION PATTERN FOR HLA SPECIFICITIES IN THE PATIENTS WITH ACUTE MYELOID LEUKEMIA." Medical Immunology (Russia) 21, no. 5 (December 13, 2019): 965–72. http://dx.doi.org/10.15789/1563-0625-2019-5-965-972.

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The article presents a study on the distribution of gene polymorphisms in the histocompatibility antigens among the patients diagnosed with AML, and healthy donors in the Republic of Kazakhstan, as well as features of the HLA-A*, *B, Cw*, DRB1*, DQB1* distribution among the patients with acute myeloid leukemia (AML). HLA typing and data processing were performed at the Research and Production Center of Transfusiology, Nur-Sultan. A total of 3808 people were examined, including 3621 healthy blood donors and 187 patients diagnosed with AML. Genomic DNA for HLA typing was isolated from peripheral blood leukocytes by proteinase method using columns with silica membrane and using a set of reagents PROTRANS DNA BOX (Protrans, Germany). Typing of HLA-A, B, C, DRB1, DQB1 in the patients and blood donors was performed by polymerase chain reaction using commercial reagent kits from Protrans (PROTRANS HLA- A*/B*/DRB1* Cyclerplate System, PROTRANS HLA-C* Cyclerplate System, PROTRANS HLA-DQB1* Cyclerplate System).HLA-A*31 (OR = 1.8; CI 1.16-2.79; p < 0.01) proved to be more common in the group of patients compared to the control group, which suggesting an association between AML and presence of this antigen. The control group showed an increased frequency of HLA-A*02 antigen (OR = 0.55; CI 0.41-0.75; p < 0.01). This antigen may be, therefore, exert a protective effect in AML development.The studies of major histocompatibility complex which include HLA genes, did significantly expanded the understanding of HLA antigens which may have strong associative links with distinct diseases, and moderately or poorly expressed links in other disorders. Analysis of the literature data showed that myeloid leukemia is characterized by decreased frequency of HLA-B13, B14, B40 antigens, most often determined by antigens B16, Bw 22, B27. In this study, HLA-A*31, B*37 were associated with AML. Phenotypes with antigens HLA-A*02, B*27, C*02, DRB1*01, *04, DQB1*06 have a probable protective effect on the development of this pathology.The study has determined some features of histocompatibility gene distribution in AML patients, detection of HLA-markers that determine the risk or resistance to the occurrence of this disease. We have established characteristic specific markers of HLA system among AML patients in Kazakhstan, which may be associated with higher risk of the disease.

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Romanyuk, D. S., A. M. Pilunov, G. A. Efimov, A. V. Bogolyubova, and E. N. Parovichnikova. "Minor histocompatibility antigens represented in HLA-A*02:01 and their search strategies." Oncohematology 18, no. 3 (September 13, 2023): 115–24. http://dx.doi.org/10.17650/1818-8346-2023-18-3-115-124.

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Minor histocompatibility antigens (MiHAs) are polymorphic peptides on the cell surface derived from self-proteins that are capable to induce an immune response during allogeneic hematopoietic stem cells transplantation. Their presentation occurs in the context of the certain major histocompatibility complex (HLA – human leucocyte antigen) alleles. One of the most common HLA alleles is HLA-A*02:01. Accordingly, for a significant number of donors and recipients pairs, it is possible to use the MiHAs presented in the HLA-A*02:01 as a target for relapsed leukemia therapy. This review discusses the main known MiHAs presented in the context of HLA-A*02:01, their characteristics and approaches used for identification. The described approaches may be used to search for new MiHAs for immunotherapy.

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Stern, Martin, Loredana Ruggeri, Marusca Capanni, Antonella Mancusi, and Andrea Velardi. "Human leukocyte antigens A23, A24, and A32 but not A25 are ligands for KIR3DL1." Blood 112, no. 3 (August 1, 2008): 708–10. http://dx.doi.org/10.1182/blood-2008-02-137521.

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Abstract Inhibitory killer cell immunoglobulin receptors (KIR) bind to major histocompatibility complex antigens. Concise knowledge of KIR ligands allows prediction of natural killer (NK)–cell alloreactivity after hematopoietic stem cell transplantation. KIR3DL1 binds to the Bw4 epitope on HLA-B antigens. Although the same epitope is also found on 4 HLA-A antigens (HLA-A23/24/25/32), these are not currently regarded as KIR3DL1 ligands. We show that expression of HLA A*2301, A*2402, or A*3201 but not HLA A*2501 protects target cells from lysis by KIR3DL1+ NK cells. KIR3DL1+ NK cells from donors expressing the Bw4 epitope on an HLA-A antigen only are fully functional and capable of lysing Bw4− target cells. HLA A25 differs at amino acid 90, close to the serologic Bw4 epitope, from A23/24/32 and from Bw4+ HLA-B antigens. These data suggest that HLA-A antigens should be taken into consideration when assessing the potential for NK alloreactivity after hematopoietic stem cell transplantation.

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Kolyubaeva, Svetlana N., Liliya A. Myakoshina, Marina I. Eliseeva, and Ruslan I. Glushakov. "HLA typing methods used for organ and tissue transplantation." Russian Military Medical Academy Reports 40, no. 2 (July 14, 2021): 21–32. http://dx.doi.org/10.17816/rmmar81197.

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The antigen system on the surface of human cells is responsible for recognizing foreign antigens. In organ transplantation, the immune system reacts to all foreign antigens that are different from the recipients antigens. In practice, solid organ transplantation is carried out with varying degrees of genetic discrepancy, while the main principle that should be followed to prevent acute and chronic transplant rejection reactions is to avoid unacceptable discrepancies. As a result, the diagnosis of typing genes of histocompatibility allows you to select a donor to which the recipient will not have sensitization. The article presents an analysis of various methods for typing human histocompatibility genes for organ and tissue transplantation. The discovery of the polymerase chain reaction was a new stage in the typing of human histocompatibility genes, which made it possible to develop new methods of gene typing. As a result, methods have been developed for typing genes using sequencers, including a new-generation MiSeq sequencer (Illumina, USА), a Massarray genomic time-of-flight analyzer (Agena Bioscience, USA). The use of sequencing has led to the possibility of simultaneous typing from 24 to 100 DNA samples. Modern technological solutions have made it possible to improve the 3rd generation NGS sequencers and provide a maximum productivity of up to 30 billion nucleotides per run, minimize restrictions on the length of DNA readings, as well as track parameters, control the sequencing process and conduct base-scaling in real time. Modern data using rapid genes typing of the human histocompatibility system (MinION Oxford nanopore) meet the needs of particularly sensitive recipients. Preliminary evidence suggests that this method will be more economical and efficient and will replace all previous ones over time (8 figs, bibliography: 40 refs).

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Vogt, M. H. J., R. A. de Paus, P. J. Voogt, R. Willemze, and J. H. F. Falkenburg. "DFFRY codes for a new human male-specific minor transplantation antigen involved in bone marrow graft rejection." Blood 95, no. 3 (February 1, 2000): 1100–1105. http://dx.doi.org/10.1182/blood.v95.3.1100.003k42_1100_1105.

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Graft rejection after histocompatibility locus antigen (HLA)-identical stem cell transplantation results from the recognition of minor histocompatibility antigens on donor stem cells by immunocompetent T lymphocytes of recipient origin. T-lymphocyte clones that specifically recognize H-Y epitopes on male target cells have been generated during graft rejection after sex-mismatched transplantation. Previously, 2 human H-Y epitopes derived from the same SMCY gene have been identified that were involved in bone marrow graft rejection. We report the identification of a new male-specific transplantation antigen encoded by the Y-chromosome-specific gene DFFRY. The DFFRY-derived peptide was recognized by an HLA-A1 restricted CTL clone, generated during graft rejection from a female patient with acute myeloid leukemia who rejected HLA-phenotypically identical bone marrow from her father. The identification of this gene demonstrates that at least 2 genes present on the human Y-chromosome code for male-specific transplantation antigens.

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Kao, KJ, DJ Cook, and JC Scornik. "Quantitative analysis of platelet surface HLA by W6/32 anti-HLA monoclonal antibody." Blood 68, no. 3 (September 1, 1986): 627–32. http://dx.doi.org/10.1182/blood.v68.3.627.627.

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Abstract Class I molecules of human major histocompatibility complex (HLA) are the most important antigenic system in determining the survival of transfused platelets in alloimmunized patients. Platelets with reduced expression of a specific type of HLA antigen may escape specific anti- HLA antibody-mediated destruction. By using 125I-labeled Fab fragments of W6/32 anti-HLA monoclonal antibody and competitive protein binding assays, we measured the range of total HLA concentrations on platelets. In 12 individuals examined, the mean number of HLA-A, B, and C molecules per platelet was 81,587 +/- 20,016 (mean +/- SD); its range was between 54,782 to 116,185 molecules per platelet. After treatment with chloroquine, 79.9 +/- 7.0% (mean +/- SD, n = 6) of HLA antigens were removed from platelets as determined by binding of 125I-W6/32 Fab. A similar result was obtained when HLA antigens on chloroquine-treated platelets were evaluated with immunofluorescence flow cytometry. In contrast, chloroquine treatment did not remove integral membrane protein such as P1A1 antigens on platelets. The presence of HLA antigens in the chloroquine eluate of platelets could be demonstrated to contain HLA antigens similar in mol wts to intact class I molecules by an immunoblotting technique. These data suggest that 70% to 80% of platelet HLA antigens are adsorbed and that such HLA antigens are not proteolytic products of integral membrane class I molecules. The origin of the adsorbed platelet HLA-antigens remains to be determined.

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Kao, KJ, DJ Cook, and JC Scornik. "Quantitative analysis of platelet surface HLA by W6/32 anti-HLA monoclonal antibody." Blood 68, no. 3 (September 1, 1986): 627–32. http://dx.doi.org/10.1182/blood.v68.3.627.bloodjournal683627.

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Class I molecules of human major histocompatibility complex (HLA) are the most important antigenic system in determining the survival of transfused platelets in alloimmunized patients. Platelets with reduced expression of a specific type of HLA antigen may escape specific anti- HLA antibody-mediated destruction. By using 125I-labeled Fab fragments of W6/32 anti-HLA monoclonal antibody and competitive protein binding assays, we measured the range of total HLA concentrations on platelets. In 12 individuals examined, the mean number of HLA-A, B, and C molecules per platelet was 81,587 +/- 20,016 (mean +/- SD); its range was between 54,782 to 116,185 molecules per platelet. After treatment with chloroquine, 79.9 +/- 7.0% (mean +/- SD, n = 6) of HLA antigens were removed from platelets as determined by binding of 125I-W6/32 Fab. A similar result was obtained when HLA antigens on chloroquine-treated platelets were evaluated with immunofluorescence flow cytometry. In contrast, chloroquine treatment did not remove integral membrane protein such as P1A1 antigens on platelets. The presence of HLA antigens in the chloroquine eluate of platelets could be demonstrated to contain HLA antigens similar in mol wts to intact class I molecules by an immunoblotting technique. These data suggest that 70% to 80% of platelet HLA antigens are adsorbed and that such HLA antigens are not proteolytic products of integral membrane class I molecules. The origin of the adsorbed platelet HLA-antigens remains to be determined.

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Ismagilov, S. M. "Distribution of histocompatibility antigens among patients with otosclerosis." Kazan medical journal 76, no. 1 (January 15, 1995): 19–22. http://dx.doi.org/10.17816/kazmj80089.

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HLA-A-B-C phenotypes in 105 patients with otosclerosis, verificated during operation and correlated with the results of histoiden- tification of 113 healthy persons are determined. It is suggested that the ethnic sign does not influence the formation of the peculiarities of HLA polymorphism. The patients were devided into two groups: with familial predisposition to otosclerosis (33) and without it (72). A2, В12, Bx, Cx antigens are more frequent among them and A28, В18, B27, B40 and Cwl are less common. The associations, intending among the patients, are absent in patients with familial agrgation. The conclusions are made of the absence of the HLA-association of familial forms of otosclerosis and the existence of the gene, determinating the stability to the development of otosclerosis (HLA-B40). It is not inconceivable that genes exist, predisposing to the development of infamilial form of the disease (B12).

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Jäger, Elke, Yao-Tseng Chen, Jan W. Drijfhout, Julia Karbach, Mark Ringhoffer, Dirk Jäger, Michael Arand, et al. "Simultaneous Humoral and Cellular Immune Response against Cancer–Testis Antigen NY-ESO-1: Definition of Human Histocompatibility Leukocyte Antigen (HLA)-A2–binding Peptide Epitopes." Journal of Experimental Medicine 187, no. 2 (January 19, 1998): 265–70. http://dx.doi.org/10.1084/jem.187.2.265.

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A growing number of human tumor antigens have been described that can be recognized by cytotoxic T lymphocytes (CTLs) in a major histocompatibility complex (MHC) class I–restricted fashion. Serological screening of cDNA expression libraries, SEREX, has recently been shown to provide another route for defining immunogenic human tumor antigens. The detection of antibody responses against known CTL-defined tumor antigens, e.g., MAGE-1 and tyrosinase, raised the question whether antibody and CTL responses against a defined tumor antigen can occur simultaneously in a single patient. In this paper, we report on a melanoma patient with a high-titer antibody response against the “cancer–testis” antigen NY-ESO-1. Concurrently, a strong MHC class I–restricted CTL reactivity against the autologous NY-ESO-1–positive tumor cell line was found. A stable CTL line (NW38-IVS-1) was established from this patient that reacted with autologous melanoma cells and with allogeneic human histocompatibility leukocyte antigen (HLA)-A2−, NY-ESO-1–positive, but not NY-ESO-1–negative, melanoma cells. Screening of NY-ESO-1 transfectants with NW38-IVS-1 revealed NY-ESO-1 as the relevant CTL target presented by HLA-A2. Computer calculation identified 26 peptides with HLA-A2–binding motifs encoded by NY-ESO-1. Of these, three peptides were efficiently recognized by NW38-IVS-1. Thus, we show that antigen-specific humoral and cellular immune responses against human tumor antigens may occur simultaneously. In addition, our analysis provides a general strategy for identifying the CTL-recognizing peptides of tumor antigens initially defined by autologous antibody.

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GÖNEN, Sevim, Sinan SARI, Yaşar KANDUR, Buket DALGIÇ, and Oğuz SÖYLEMEZOĞLU. "EVALUATION OF HUMAN LEUKOCYTE ANTIGEN CLASS I AND II ANTIGENS IN HELICOBACTER PYLORI-POSITIVE PEDIATRIC PATIENTS WITH ACTIVE GASTRITIS AND DUODENAL ULCER." Arquivos de Gastroenterologia 54, no. 4 (October 2, 2017): 297–99. http://dx.doi.org/10.1590/s0004-2803.201700000-62.

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ABSTRACT BACKGROUND: As being the first bacteria determined to be carcinogenic, Helicobacter pylori (H. pylori) is a pathogen localized in the stomach in more than half of the world population. Some earlier studies have found a relation between tissue histocompatibility antigens and gastric cancers depending on the regions. OBJECTIVE: The present study aimed to determine the distribution of human leukocyte antigen (HLA) class I and class II antigens in H. pylori-positive pediatric patients with active gastritis and duodenal ulcer, excluding cancer cases, in our center. METHODS: The study included 40 patients diagnosed with H. pylori-positive active gastritis and duodenal ulcer and 100 controls consisting of healthy donor candidates. The HLA class I and class II antigens were studied in the isolated DNA samples using the polymerase chain reaction sequence-specific oligonucleotide probes. RESULTS: The frequency of HLA-B*51 antigen was significantly higher in the patient group than in the control group (40% vs 17%; P=0.003). There was no difference between the two groups in terms of the frequencies of HLA-A, HLA-C, HLA-DR, and HLA-DQ antigens. CONCLUSION: It was determined that HLA-B*51 plays a critical role in H. pylori infection.

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Chersi, Alberto, Richard A. Houghten, Maria C. Morganti, and Eleonora Muratti. "Recognition of HLA Class II Molecules by Antipeptide Antibodies Elicited by Synthetic Peptides Selected from Regions of HLA-DP Antigens." Zeitschrift für Naturforschung C 42, no. 11-12 (December 1, 1987): 1313–18. http://dx.doi.org/10.1515/znc-1987-11-1227.

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Repeated immunizations of rabbits with chemically synthesized peptides from selected regions of HLA-DP histocompatibility antigens resulted in the production of specific antibodies that were then isolated from the immune sera by chromatography on Sepharose-peptide immunoadsorbents. The purified antibodies, when tested with an enzyme-linked immunosorbant assay, specifically bound to the inciting fragments; moreover, two of them recognized glycoproteins extracted by nonionic detergents from human chronic lymphocytic leukemia cells, as revealed by binding assays. The results suggest that amino acid stretches 51 - 61 of the alpha chain and 80-90 of the beta chain of HLA-DP histocompatibility antigens are likely exposed on the surface of the protein molecule. The specific recognition of DP regions is strongly suggested by the difference in the binding of those antibodies to soluble membrane proteins, as compared to the binding of monomorphic anti-Class II monoclonal antibodies to the same antigens.

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Berard, Frederic, Patrick Blanco, Jean Davoust, Eve-Marie Neidhart-Berard, Mahyar Nouri-Shirazi, Nicolas Taquet, Donata Rimoldi, Jean Charles Cerottini, Jacques Banchereau, and A. Karolina Palucka. "Cross-Priming of Naive Cd8 T Cells against Melanoma Antigens Using Dendritic Cells Loaded with Killed Allogeneic Melanoma Cells." Journal of Experimental Medicine 192, no. 11 (November 27, 2000): 1535–44. http://dx.doi.org/10.1084/jem.192.11.1535.

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The goal of tumor immunotherapy is to elicit immune responses against autologous tumors. It would be highly desirable that such responses include multiple T cell clones against multiple tumor antigens. This could be obtained using the antigen presenting capacity of dendritic cells (DCs) and cross-priming. That is, one could load the DC with tumor lines of any human histocompatibility leukocyte antigen (HLA) type to elicit T cell responses against the autologous tumor. In this study, we show that human DCs derived from monocytes and loaded with killed melanoma cells prime naive CD45RA+CD27+CD8+ T cells against the four shared melanoma antigens: MAGE-3, gp100, tyrosinase, and MART-1. HLA-A201+ naive T cells primed by DCs loaded with HLA-A201− melanoma cells are able to kill several HLA-A201+ melanoma targets. Cytotoxic T lymphocyte priming towards melanoma antigens is also obtained with cells from metastatic melanoma patients. This demonstration of cross-priming against shared tumor antigens builds the basis for using allogeneic tumor cell lines to deliver tumor antigens to DCs for vaccination protocols.

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Versteeg, R., K. M. Krüse-Wolters, A. C. Plomp, A. van Leeuwen, N. J. Stam, H. L. Ploegh, D. J. Ruiter, and P. I. Schrier. "Suppression of class I human histocompatibility leukocyte antigen by c-myc is locus specific." Journal of Experimental Medicine 170, no. 3 (September 1, 1989): 621–35. http://dx.doi.org/10.1084/jem.170.3.621.

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The c-myc oncogene downregulates class I HLA expression in human melanoma. The major class I HLA antigens are encoded by three loci, A, B, and C, and we investigated whether these loci are suppressed equally by c-myc. In three melanoma cell lines with high c-myc expression, we analyzed mRNA, protein, and cell surface expression of the class I HLA antigens. Whereas the HLA-B locus expression was found to be strongly reduced, the HLA-A locus was expressed normally. Analysis of c-myc-transfected clones of two melanoma cell lines confirmed that c-myc preferentially suppresses the class I HLA-B locus. Immunohistochemical analysis of fresh melanoma lesions also showed that in the tumors the HLA-A loci are expressed normally, while on the majority of tumor cells no HLA-B antigen expression was found. This downregulation may have consequences for the recognition of malignant cells by tumor-infiltrating lymphocytes. Our results predict that HLA-B-restricted cytotoxic T cells will be unable to kill high c-myc-expressing melanoma cells.

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Anderson, D. J., and R. S. Berkowitz. "Gamma-interferon enhances expression of Class I MHC antigens in the weakly HLA+ human choriocarcinoma cell line BeWo, but does not induce MHC expression in the HLA- choriocarcinoma cell line Jar." Journal of Immunology 135, no. 4 (October 1, 1985): 2498–501. http://dx.doi.org/10.4049/jimmunol.135.4.2498.

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Abstract PHA-activated lymphocyte supernatants and high doses of affinity-purified human gamma-interferon enhance the expression of apparently normal Class I histocompatibility antigens in a malignant human trophoblast cell line that expresses low amounts of these antigens under normal culture conditions. Another human choriocarcinoma cell line, Jar, which is normally HLA-, did not respond to this treatment. This system provides a model in which to study further the regulation and effects of MHC antigen expression in cells of trophoblastic origin.

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van der Harst, D., E. Goulmy, JH Falkenburg, YM Kooij-Winkelaar, SA van Luxemburg- Heijs, HM Goselink, and A. Brand. "Recognition of minor histocompatibility antigens on lymphocytic and myeloid leukemic cells by cytotoxic T-cell clones." Blood 83, no. 4 (February 15, 1994): 1060–66. http://dx.doi.org/10.1182/blood.v83.4.1060.1060.

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Abstract Clinical studies indicated an enhanced antileukemic effect of allogeneic bone marrow transplantation (BMT), as compared with autologous BMT. After allogeneic HLA-identical BMT, donor-derived cytotoxic T lymphocytes (CTLs) directed at minor histocompatibility (mH) antigens on the recipients, tissues can be shown. To evaluate the antileukemic reactivity of mH antigen-specific CTLs, we analyzed the expression of mH antigens on circulating lymphocytic and myeloid leukemic cells. We show that the defined mH specificities HA-1 through HA-5 and H-Y are present on leukemic cells, indicating that mH antigen- specific CTLs are capable of HLA class I-restricted antigen-specific lysis of leukemic cells. Compared with interleukin-2-stimulated normal lymphocytes, leukemic cells of lymphocytic origin are less susceptible to T-cell-mediated cytotoxicity by the HA-2 mH antigen-specific CTL and the anti-HLA-A2 CTL clone. A possible explanation for this phenomenon is impaired expression of the LFA-1 adhesion molecule. Our study suggests that mH antigen-specific HLA class I-restricted CD8+ CTLs may be involved in the graft-versus-leukemia reactivity after allogeneic BMT.

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van der Harst, D., E. Goulmy, JH Falkenburg, YM Kooij-Winkelaar, SA van Luxemburg- Heijs, HM Goselink, and A. Brand. "Recognition of minor histocompatibility antigens on lymphocytic and myeloid leukemic cells by cytotoxic T-cell clones." Blood 83, no. 4 (February 15, 1994): 1060–66. http://dx.doi.org/10.1182/blood.v83.4.1060.bloodjournal8341060.

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Clinical studies indicated an enhanced antileukemic effect of allogeneic bone marrow transplantation (BMT), as compared with autologous BMT. After allogeneic HLA-identical BMT, donor-derived cytotoxic T lymphocytes (CTLs) directed at minor histocompatibility (mH) antigens on the recipients, tissues can be shown. To evaluate the antileukemic reactivity of mH antigen-specific CTLs, we analyzed the expression of mH antigens on circulating lymphocytic and myeloid leukemic cells. We show that the defined mH specificities HA-1 through HA-5 and H-Y are present on leukemic cells, indicating that mH antigen- specific CTLs are capable of HLA class I-restricted antigen-specific lysis of leukemic cells. Compared with interleukin-2-stimulated normal lymphocytes, leukemic cells of lymphocytic origin are less susceptible to T-cell-mediated cytotoxicity by the HA-2 mH antigen-specific CTL and the anti-HLA-A2 CTL clone. A possible explanation for this phenomenon is impaired expression of the LFA-1 adhesion molecule. Our study suggests that mH antigen-specific HLA class I-restricted CD8+ CTLs may be involved in the graft-versus-leukemia reactivity after allogeneic BMT.

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Yagüe, Jesús, Iñaki Alvarez, Didier Rognan, Manuel Ramos, Jesús Vázquez, and José A. López de Castro. "An N-Acetylated Natural Ligand of Human Histocompatibility Leukocyte Antigen (Hla)-B39." Journal of Experimental Medicine 191, no. 12 (June 12, 2000): 2083–92. http://dx.doi.org/10.1084/jem.191.12.2083.

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Sequence-independent interactions involving the free peptidic NH2 terminus are thought to be an essential feature of peptide binding to classical major histocompatibility complex (MHC) class I proteins. Challenging this paradigm, a natural Nα-acetylated ligand of human histocompatibility leukocyte antigen (HLA)-B39 was identified in this study. It matched the NH2-terminal sequence of two human helicases, was resistant to aminopeptidase M, and was produced with high yield from a synthetic 30 mer with the sequence of the putative parental protein by the 20S proteasome. This is the first reported natural ligand of classical MHC class I antigens that has a blocked NH2 terminus.

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TSUJIMURA, AKIRA, SHIRO TAKAHARA, MASAYA KTTAMURA, HIDENOBU NQURA, MINORU KOGA, MASAHARU SADA, TAKAYUKI TSUJI, KIYOMI MATSUMIYA, and AKIHIKO OKUYAMA. "HLA‐DR Antigen and HLA‐DRB1 Genotyping with Nonobstructive Azoospermia in Japan." Journal of Andrology 20, no. 4 (July 8, 1999): 545–50. http://dx.doi.org/10.1002/j.1939-4640.1999.tb02554.x.

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ABSTRACT: We previously reported that the HLA‐A33, ‐B13, and ‐B44 antigens, which are major histocompatibility complex class I molecules, are involved in the susceptibility of nonobstructive azoospermia in Japanese men. In this report, HLA‐DR antigens, which are class II molecules, are investigated by advanced DNA typing in addition to classical serological typing to study a more complex genotype of HLA‐DRB2. Genotyping was performed by the polymerase chain reaction‐sequence‐specific primer (PCR‐SSP) method of analysis and/or by a commercial rapid assay based on the polymerase chain reaction (PCR), followed by reverse dotblot hybridization of PCR products (the Inno‐LiPA assay). The allele frequencies of the HLA‐DR13 antigen and the ‐DRB1*1302 allele were significantly higher in Japanese subjects with nonobstructive azoospermia compared with a control group of healthy Japanese men, and these alleles were associated with relative risks for nonobstructive azoospermia of 4.2 and 4.9, respectively. If we suppose this strong linkage to both HLA class I and II antigens is due to linkage disequilibrium, it may suggest the existence of a novel gene involved in spermatogenesis in the class III region, which is located between the class I and class II regions and contains several genes other than HLA.

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Dohr, G. A., W. Motter, S. Leitinger, G. Desoye, W. Urdl, R. Winter, M. M. Wilders-Truschnig, B. Uchanska-Ziegler, and A. Ziegler. "Lack of expression of HLA [corrected] class I and class II molecules on the human oocyte." Journal of Immunology 138, no. 11 (June 1, 1987): 3766–70. http://dx.doi.org/10.4049/jimmunol.138.11.3766.

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Abstract The expression of histocompatibility leukocyte antigen (HLA) class I and class II antigens on human oocytes was investigated by the indirect immunofluorescence assay using well-defined monoclonal antibodies. Oocytes were obtained from an in vitro fertilization program or were studied on frozen sections from human ovaries. Neither HLA class I, beta 2-microglobulin, nor HLA class II molecules were detected on cultured oocytes or frozen sections. The zona pellucida also lacked these antigens, but granulosa cells expressed HLA class I molecules. Our results also indicate the presence of certain types of class II molecules on granulosa cells. The present experiments demonstrate that the human oocyte belongs to those few cell types in the human body which are devoid of both types of HLA molecules.

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Olsen, Kelly Shea, Hancong Tang, Junke Wang, Sarah Entwistle, Dante S. Bortone, Steven Vensko, Loreall Pooler, et al. "Population Distribution of GvL and GvH Minor Histocompatibility Antigens." Blood 136, Supplement 1 (November 5, 2020): 23–25. http://dx.doi.org/10.1182/blood-2020-141120.

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Background: Donor-derived T cells that target minor histocompatibility antigens (mHAs) in allogeneic hematopoietic cell transplant (HCT) mediate graft versus leukemia (GvL) and graft versus host (GvH) effects. Prediction of mHAs that drive GvL has garnered interest for targeted immunotherapy, but there have been few large-scale studies of population prevalence of predicted mHAs. Prioritization of mHAs that are shared among patients would allow for treatment of more individuals with mHA-targeting therapies. We report here population metrics of predicted mHAs in a dataset of over 3000 patients treated with HCT and reported to CIBMTR from 2000-2011. Our goal is to identify the most common mHAs within leukemia and Myelodysplastic Syndrome (MDS) patient populations to target with T cell immunotherapies or graft engineering techniques. Methods: Data is derived from two cohorts of donor recipient HCT pairs (DRPs) treated for Acute Myeloid Leukemia (AML), Acute Lymphocytic Leukemia (ALL), and MDS from the CIBMTR and previously analyzed in DISCOVeRY-BMT. Cohort 1 included 2609 10/10 HLA-matched DRPs treated from 2000-2008, and Cohort 2 included 572 10/10 HLA-matched DRPs treated from 2009-2011 plus 351 8/8 HLA-matched DRPs treated from 2000-2011 (Hahn et al. 2015, Biol Blood Marrow Transplant). Cohorts were combined for analyses. Approximately 20,000 missense SNPs were extracted from Illumina HumanOmni Express genotyping data. Computational mHA prediction was performed according to prior work from our lab (Lansford et al. 2018, Blood Adv.). Minor mismatches were predicted based on coding SNPs present in the recipient but not donor. mHAs were defined as mismatches that would lead to variant peptides predicted to bind at least 1 recipient HLA molecule and be expressed in leukemia cells (GvL mHA) and/or acute GvHD target organs (GvH mHA). GvL mHAs were categorized as "GvL,No_GvH" or "GvL" based on transcripts per million (TPM) corresponding to GvH organs, with "GvL" indicating between 5-50 TPM and "GvL,No_GvH" indicating <5 TPM. GvH mHAs were categorized similarly with respect to expression in leukemia cells. "GvL,GvH" indicated mHAs expressed highly in both leukemia and in GvHD target organs. Results: Patient demographics and number of total predicted mHAs from each ethnic group are shown in Table 1. Number of predicted mHAs per patient varied widely both within and between HLA types (Figure 1). Despite underrepresentation of some ethnic groups in our dataset, we identified thousands of potential mHAs in each group (Figure 2A). GvL mHA and GvH mHA proportions were similar across recipient ethnicities (Figure 2A-B). GvL mHA made up approximately half of predicted mHAs for each ethnic group (Figure 2B). Total numbers of mHAs per HCT recipient were significantly different between recipient ethnic groups within each cohort (Figure 2C). Although proportions of GvL vs GvH mHAs were stable across HLA alleles, there were substantial differences in number of predicted mHA by allele (Figure 3). Despite limited representation of some HLA types in our dataset, we were able to identify GvL mHAs for potential therapeutic targeting corresponding to 56 HLA alleles. We generated ranked lists of the most common shared mHA for each HLA allele, using an implementation of the standard greedy algorithm solution to the maximum set coverage problem. With this method, we identified the fewest number of mHA peptides needed to cover desired percentages of the recipient population with at least one mHA. For example, for HLA A*02:01, HLA*B07:02, and HLA*C07:01, engineering T cells to target the top nine to twelve peptides would allow for treatment of 80% of the patient population in our cohorts (Figure 4). These represent common HLA alleles in Caucasian, African American, Hispanic, and Asian populations, indicating that this technique can identify targets that could be therapeutically beneficial for a greater diversity of patients than standard treatments. mHA pools can also be filtered on peptide expression or HLA binding to ensure that the targeted peptides are highly expressed and presented. Conclusions: Despite differences in predicted number of mHA by ethnicity and HLA alleles, shared GvL mHA exist across common HLA. To the extent that these are targetable by adoptive cellular therapy, we can expand equal access to mHA targeted immunotherapies, improving upon traditional models where only the most prevalent HLA types are covered. Disclosures Armistead: Cell Microsystems: Patents & Royalties: Patent application U.S. 16/347,104 "Automated collection of a specified number of cells"; GeneCentric: Consultancy. Vincent:GeneCentric Therapeutics: Consultancy.

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OLIVIUS, ESKIL, and WERNER POLLAND. "HISTOCOMPATIBILITY (HLA) ANTIGENS IN CAPSULAR GLAUCOMA AND SIMPLEX GLAUCOMA." Acta Ophthalmologica 58, no. 3 (May 27, 2009): 406–10. http://dx.doi.org/10.1111/j.1755-3768.1980.tb05740.x.

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Chaux, Pascal, Valérie Vantomme, Vincent Stroobant, Kris Thielemans, Jurgen Corthals, Rosalie Luiten, Alexander M. M. Eggermont, Thierry Boon, and Pierre van der Bruggen. "Identification of MAGE-3 Epitopes Presented by HLA-DR Molecules to CD4+ T Lymphocytes." Journal of Experimental Medicine 189, no. 5 (March 1, 1999): 767–78. http://dx.doi.org/10.1084/jem.189.5.767.

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MAGE-type genes are expressed by many tumors of different histological types and not by normal cells, except for male germline cells, which do not express major histocompatibility complex (MHC) molecules. Therefore, the antigens encoded by MAGE-type genes are strictly tumor specific and common to many tumors. We describe here the identification of the first MAGE-encoded epitopes presented by histocompatibility leukocyte antigen (HLA) class II molecules to CD4+ T lymphocytes. Monocyte-derived dendritic cells were loaded with a MAGE-3 recombinant protein and used to stimulate autologous CD4+ T cells. We isolated CD4+ T cell clones that recognized two different MAGE-3 epitopes, MAGE-3114–127 and MAGE-3121–134, both presented by the HLA-DR13 molecule, which is expressed in 20% of Caucasians. The second epitope is also encoded by MAGE-1, -2, and -6. Our procedure should be applicable to other proteins for the identification of new tumor-specific antigens presented by HLA class II molecules. The knowledge of such antigens will be useful for evaluation of the immune response of cancer patients immunized with proteins or with recombinant viruses carrying entire genes coding for tumor antigens. The use of antigenic peptides presented by class II in addition to peptides presented by class I may also improve the efficacy of therapeutic antitumor vaccination.

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Sultana, Sharmin, Shahina Tabassum, and Afzalun Nessa. "Human Leukocyte Antigen: Class I Allele Frequencies and Haplotype Distributionin a Tertiary Care Hospital in Bangladesh." Bangladesh Medical Research Council Bulletin 44, no. 1 (June 6, 2018): 1–8. http://dx.doi.org/10.3329/bmrcb.v44i1.36798.

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Human leukocyte antigen (HLA) are cell surface glycoproteins encoded by Major Histocompatibility Complex (MHC) geneof human genome. HLA antigen frequency and haplotype distribution are useful for determining disease associations, origin, migration and genetic relationships between populations and predicting the outcome of transplantation. Thus, the present study was carried outto identify HLA class I (HLA-A and HLA-B) antigen and haplotype distribution among a selected Bangladeshi population. This retrospective study was conducted among 1070 individuals who were referred by cliniciansfor HLA typing at the Tissue Typing Laboratory of the Department of Virology, Bangabandhu Sheikh Mujib Medical University (BSMMU) during the period 2009 to 2011. For HLA typing, Blood was collected in heparin containing tube and the laboratory tests were performed by the microlymphocytotoxicity technique according to manufacturer’s instructions.Out of 19 HLA-A and 37HLA-B antigens tested, a total of 19/19 and 36/37 antigens were detectedrespectively in this study. The most frequent antigens of HLA-A and HLA-B detected were A11 (25.4%), A24 (16.6%), B75 (18.1%) and B35 (11.3%). The least antigen frequency detected for HLA-A locus were A69 (0.09%), A26 (0.28%), A34 (0.28%), while for HLA-B locus were B81 (0.09%) and B56 (0.09%). Among the HLA-A and HLA-B antigens, some alleles were found to be homozygote such as A11 (4.0%), A2 (2.7%), A24 (2.1%) andB75 (2.4%), B35 (1.8%), and B44 (1.4%) respectively. The most frequent haplotype in the study populationwereA11: B75 (4.9%). The most frequent antigens of HLA-A and HLA-B detected were A11 (25.4%), B75 (18.1%) respectively. The distribution of HLA haplotypes among the study population indicates that it has the influence of Oriental and Asian populations. Thus, this study will be helpful to provide valuable information for population genetics and HLA disease association analysis.Bangladesh Med Res Counc Bull 2018; 44(1):01-08

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Severinsson, L., I. Martens, and P. A. Peterson. "Differential association between two human MHC class I antigens and an adenoviral glycoprotein." Journal of Immunology 137, no. 3 (August 1, 1986): 1003–9. http://dx.doi.org/10.4049/jimmunol.137.3.1003.

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Abstract The glycoprotein E19, encoded in early region 3 of adenovirus-2, forms complexes with major histocompatibility complex class I antigens. As a result of the complex formation, the intracellular transport of the class I antigens is abrogated, and adenovirus-infected cells display gradually diminishing quantities of cell surface-expressed class I molecules. To assess whether the E19 protein interacts equally well with different class I antigens, the associations between the viral protein and HLA-A2 and HLA-B7 antigens have been estimated. By infecting transfected HeLa cells expressing various amounts of HLA-A2 and HLA-B7 molecules, respectively, with various infectious doses of adenovirus-2, experimental conditions could be established that allowed quantitative estimates of the interactions to be determined. It was found that HLA-A2 molecules and the E19 protein interacts with a binding constant that is more than twice as high as that for HLA-B7 antigens and the viral protein. It is suggested that the pathogenicity of the virus may be dependent on the HLA-type of the infected individual.

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Tilkin, A. F., M. Bagot, M. Kayibanda, J. P. Vernant, and J. P. Levy. "A human autoreactive T cell line specific for minor histocompatibility antigen(s) isolated from a bone marrow-grafted patient." Journal of Immunology 137, no. 12 (December 15, 1986): 3772–76. http://dx.doi.org/10.4049/jimmunol.137.12.3772.

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Abstract A human autoreactive T cell line named Bur-1 has been obtained from a woman 4 mo after an allogeneic bone marrow transplantation (BMT) from one of her HLA-identical brothers. The phenotype of the cell line is 100% T11+ and over 90% T4+, and the karyotype confirms its donor (male) origin. These donor T cells proliferate specifically in the presence of donor's peripheral blood monocytes (PBM) but not recipient's cells, and they kill specifically donor's but not recipient's Epstein-Barr virus (EBV)-induced lymphoblastoid cell lines (LCL). PBM from another HLA-identical brother and from several unrelated donors also stimulate Bur-1 cells, and EBV-induced LCL from the same donors are killed in cytotoxicity assays. All of these donors share HLA-DR5 or HLA-DRw11 (the major split of HLA-DR5) with Bur-1 cells. However, some but not all of the PBM sharing HLA-DR5 with Bur-1 cells are recognized. Therefore, in contrast with the previously described autoreactive T cells, Bur-1 cells are not directed against self-MHC antigens but rather recognize autologous minor histocompatibility (mH) antigens in the context of autologous HLA class II molecules. Because both male and female cells can be recognized, the reacting minor antigen could not be the male-specific HY antigen. It is suggested that autoreactivity against mH antigens can be observed in bone marrow-grafted patients due to the education of bone marrow donor precursors in the recipient thymus not allowing tolerance to autologous (donor) mH antigens not shared by the recipient.

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Inman, R. D. "Immunogenetic aspects of host immune response." Canadian Journal of Microbiology 34, no. 3 (March 1, 1988): 319–22. http://dx.doi.org/10.1139/m88-058.

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The central role of histocompatibility leukocyte antigens (HLA) class II molecules in antigen presentation has received great attention in recent years, yet class I molecules have been defined as primarily functioning as a restriction element for cytotoxic T cell killing of virus-infected cells. Extensive clinical evidence, however, indicates that the HLA class I genes are strongly associated with nonseptic complications of enteric and genitourinary bacterial infections. Ninety percent of patients with Reiter's syndrome and reactive arthritis are positive for HLA-B27, yet the mechanism of disease susceptibility conferred by this gene remains obscure. Hypotheses concerning this interaction include (i) class I antigens functioning as receptors for microbial antigens; (ii) class I antigens expressing determinants that cross-react with microbial antigens; and (iii) class I genes controlling immunoregulatory functions that dictate qualitative differences in immune response to pathogenic organisms. These hypotheses await formal testing and hold great promise for understanding immunogenetic control of immune responses in general.

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Verdijk, Rob M., Antoinette Kloosterman, Jos Pool, Maarten van de Keur, Albert M. I. H. Naipal, Astrid G. S. van Halteren, Anneke Brand, Tuna Mutis, and Els Goulmy. "Pregnancy induces minor histocompatibility antigen–specific cytotoxic T cells: implications for stem cell transplantation and immunotherapy." Blood 103, no. 5 (March 1, 2004): 1961–64. http://dx.doi.org/10.1182/blood-2003-05-1625.

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AbstractRecipients of HLA-identical stem cell transplants have a poorer transplant outcome if the donor is female rather than male. We analyzed whether pregnancy primes for minor histocompatibility (H) antigens. Peripheral blood mononuclear cells (PBMCs) from healthy multiparous female blood donors were depleted for CD4+, CD14+, CD16+, and CD19+ cells, stained with minor H antigen–specific HLA-A2 tetramers, sorted by fluorescence-activated cell sorting, and tested for cytotoxic activity. Minor H antigens HY-, HA-1–, and HA-2–specific cytotoxic T cells (CD8+, CD45RA–) were present in PBMCs from 4 of 7 female donors up to 22 years after the last delivery. Interestingly, in 2 of the 4 cases microchimerism of the putative immunizing minor H antigen was observed. Thus, pregnancy can lead to alloimmune responses against the infant's paternal minor H antigens. The minor H antigen immunization status of female donors raises important questions for the clinical practice of stem cell transplantation.

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Ayala García, Marco Antonio, Beatriz González Yebra, Andrea Liliana López Flores, and Eduardo Guaní Guerra. "The Major Histocompatibility Complex in Transplantation." Journal of Transplantation 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/842141.

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The transplant of organs is one of the greatest therapeutic achievements of the twentieth century. In organ transplantation, the adaptive immunity is considered the main response exerted to the transplanted tissue, since the principal target of the immune response is the MHC (major histocompatibility complex) molecules expressed on the surface of donor cells. However, we should not forget that the innate and adaptive immunities are closely interrelated and should be viewed as complementary and cooperating. When a human transplant is performed, HLA (human leukocyte antigens) molecules from a donor are recognized by the recipient's immune system triggering an alloimmune response Matching of donor and recipient for MHC antigens has been shown to have a significant positive effect on graft acceptance. This paper will present MHC, the innate and adaptive immunities, and clinical HLA testing.

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Heemskerk, Mirjam H. M., Manja Hoogeboom, Renate Hagedoorn, Michel G. D. Kester, Roel Willemze, and J. H. Frederik Falkenburg. "Reprogramming of Virus-specific T Cells into Leukemia-reactive T Cells Using T Cell Receptor Gene Transfer." Journal of Experimental Medicine 199, no. 7 (March 29, 2004): 885–94. http://dx.doi.org/10.1084/jem.20031110.

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T cells directed against minor histocompatibility antigens (mHags) might be responsible for eradication of hematological malignancies after allogeneic stem cell transplantation. We investigated whether transfer of T cell receptors (TCRs) directed against mHags, exclusively expressed on hematopoietic cells, could redirect virus-specific T cells toward antileukemic reactivity, without the loss of their original specificity. Generation of T cells with dual specificity may lead to survival of these TCR-transferred T cells for prolonged periods of time in vivo due to transactivation of the endogenous TCR of the tumor-reactive T cells by the latent presence of viral antigens. Furthermore, TCR transfer into restricted T cell populations, which are nonself reactive, will minimize the risk of autoimmunity. We demonstrate that cytomegalovirus (CMV)-specific T cells can be efficiently reprogrammed into leukemia-reactive T cells by transfer of TCRs directed against the mHag HA-2. HA-2-TCR–transferred CMV-specific T cells derived from human histocompatibility leukocyte antigen (HLA)-A2+ or HLA-A2− individuals exerted potent antileukemic as well as CMV reactivity, without signs of anti–HLA-A2 alloreactivity. The dual specificity of these mHag-specific, TCR-redirected virus-specific T cells opens new possibilities for the treatment of hematological malignancies of HLA-A2+ HA-2–expressing patients transplanted with HLA-A2–matched or –mismatched donors.

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Manandhar, Rekha, Gaurab Pandey, Ranjan Raj Bhatta, and Runa Jha. "Analysis of Human Leukocyte Antigen Frequency among Renal Transplant Recipients and Donors in Nepal." Global Journal of Transfusion Medicine 9, no. 1 (January 2024): 57–60. http://dx.doi.org/10.4103/gjtm.gjtm_79_23.

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ABSTRACT Background and Objectives: Kidney transplants are effective for advanced renal failure, but graft rejection can occur when the recipient’s immune system misidentifies the kidney as a foreign object. Human leukocyte antigen (HLA), a component of the host’s immunological defense system, acts as a barrier to graft rejection. Selecting potential kidney recipients and donors for transplantation requires careful consideration of histocompatibility for the HLA-A, HLA-B, and HLA-DRB1 antigens. Mismatches between donors and recipients prolong transplant therapy, leading to lower graft survival and higher mortality. The objective of the study was to analyze HLA-A, HLA-B, and HLA-DRB1 antigens frequency in live-related renal transplant recipients and donors visiting the Department of Histocompatibility and Immunopathology at the National Public Health Laboratory, Teku, Kathmandu, Nepal. Methods: A retrospective study was conducted by using data from 104 renal transplant recipients and donors whose samples had previously been collected, processed, and analyzed to identify the Class I loci (HLA-A and HLA-B) and Class II loci (DRB1) between November 2021 and February 2024. Results: The study found that the majority of donors were female, and the majority of recipients were male. In this study, 10, 17, and 12 different HLA-A, B, and DRB1 alleles were found in recipients and donors. Alleles found more frequently are A*11 (25.00%), A*24 (23.08%), sB*15 (22.60%), B*35 (12.98%), DRB1*15 (22.60%), and DRB1*12 (21.63%). Conclusions: The study suggests that both donors and recipients of renal transplants in Nepal have a diverse HLA antigen distribution, which could aid in selecting a genetically closer group as potential matched donors for transplant recipients.

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Kraemer, Thomas, Rainer Blasczyk, and Christina Bade-Doeding. "HLA-E: A Novel Player for Histocompatibility." Journal of Immunology Research 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/352160.

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The classical class I human leukocyte antigens (HLA-A, -B, and -C) present allele-specific self- or pathogenic peptides originated by intracellular processing to CD8+immune effector cells. Even a single mismatch in the heavy chain (hc) of an HLA class I molecule can impact on the peptide binding profile. Since HLA class I molecules are highly polymorphic and most of their polymorphisms affect the peptide binding region (PBR), it becomes obvious that systematic HLA matching is crucial in determining the outcome of transplantation. The opposite holds true for the nonclassical HLA class I molecule HLA-E. HLA-E polymorphism is restricted to two functional versions and is thought to present a limited set of highly conserved peptides derived from class I leader sequences. However, HLA-E appears to be a ligand for the innate and adaptive immune system, where the immunological response to peptide-HLA-E complexes is dictated through the sequence of the bound peptide. Structural investigations clearly demonstrate how subtle amino acid differences impact the strength and response of the cognate CD94/NKG2 or T cell receptor.

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Yamamoto, J., A. Kariyone, N. Akiyama, K. Kano, and M. Takiguchi. "Presentation of human minor histocompatibility antigens by HLA-B35 and HLA-B38 molecules." Proceedings of the National Academy of Sciences 87, no. 7 (April 1, 1990): 2583–87. http://dx.doi.org/10.1073/pnas.87.7.2583.

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van Ham, Marieke, Marcel van Lith, Björn Lillemeier, Esther Tjin, Ulrike Grüneberg, Dinah Rahman, Liesbeth Pastoors, et al. "Modulation of the Major Histocompatibility Complex Class II–Associated Peptide Repertoire by Human Histocompatibility Leukocyte Antigen (Hla)-Do." Journal of Experimental Medicine 191, no. 7 (March 27, 2000): 1127–36. http://dx.doi.org/10.1084/jem.191.7.1127.

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Antigen presentation by major histocompatibility complex class II molecules is essential for antibody production and T cell activation. For most class II alleles, peptide binding depends on the catalytic action of human histocompatibility leukocyte antigens (HLA)-DM. HLA-DO is selectively expressed in B cells and impedes the activity of DM, yet its physiological role remains unclear. Cell surface iodination assays and mass spectrometry of major histocompatibility complex class II–eluted peptides show that DO affects the antigenic peptide repertoire of class II. DO generates both quantitative and qualitative differences, and inhibits presentation of large-sized peptides. DO function was investigated under various pH conditions in in vitro peptide exchange assays and in antigen presentation assays using DO− and DO+ transfectant cell lines as antigen-presenting cells, in which effective acidification of the endocytic pathway was prevented with bafilomycin A1, an inhibitor of vacuolar ATPases. DO effectively inhibits antigen presentation of peptides that are loaded onto class II in endosomal compartments that are not very acidic. Thus, DO appears to be a unique, cell type–specific modulator mastering the class II–mediated immune response induced by B cells. DO may serve to increase the threshold for nonspecific B cell activation, restricting class II–peptide binding to late endosomal compartments, thereby affecting the peptide repertoire.

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Zaborek-Łyczba, Monika, Jakub Łyczba, Paulina Mertowska, Sebastian Mertowski, Anna Hymos, Martyna Podgajna, Paulina Niedźwiedzka-Rystwej, and Ewelina Grywalska. "The HLA-G Immune Checkpoint Plays a Pivotal Role in the Regulation of Immune Response in Autoimmune Diseases." International Journal of Molecular Sciences 22, no. 24 (December 12, 2021): 13348. http://dx.doi.org/10.3390/ijms222413348.

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The human G-leukocyte antigen (HLA-G) molecule is a non-classical major histocompatibility complex (MHC) class I molecule. The pertinence of HLA-G has been investigated in numerous studies which have sought to elucidate the relevance of HLA-G in pathologic conditions, such as autoimmune diseases, cancers, and hematologic malignancies. One of the main goals of the current research on HLA-G is to use this molecule in clinical practice, either in diagnostics or as a therapeutic target. Since HLA-G antigens are currently considered as immunomodulatory molecules that are involved in reducing inflammatory and immune responses, in this review, we decided to focus on this group of antigens as potential determinants of progression in autoimmune diseases. This article highlights what we consider as recent pivotal findings on the immunomodulatory function of HLA-G, not only to establish the role of HLA-G in the human body, but also to explain how these proteins mediate the immune response.

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Kim, Ae, Isamu Hartman, and Scheherazade Sadegh-Nasseri. "Survival of antigenic epitope requires class II MHC capture prior to lysosomal proteolysis (93.21)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S170. http://dx.doi.org/10.4049/jimmunol.178.supp.93.21.

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Abstract The paradigmatic model for the generation of peptide determinants for class II major histocompatibility complex molecules (MHC II) is that proteolytic fragmentation of antigen precedes the capture of the resulting peptides by MHC II (cut/trim first, bind later). However, circumstantial evidence exists to support an alternate model in which MHC II binding of antigenic epitope occurs prior to the proteolytic fragmentation of that antigen (bind first, cut/trim later). To distinguish between these two models, we analyzed the interaction of HLA-DR1 with two protein antigens, type II collagen and influenza hemagglutinin. Here, using a novel cell?free antigen processing system composed solely of purified soluble protein components, HLA-DR1, two cathepsins, and HLA-DM, combined with mass spectrometric identification of the bound peptides, we demonstrate for both antigens that; the protein antigens bind MHC class II prior to digestion by lysosomal proteases,the immunodominant epitope of the antigens are degraded by lysosomal proteases if not bound to MHC class II, andthe epitopes, when bound to MHCII, are protected from proteolytic degradation. These findings conclusively support the “bind first, cut/trim later” model and have important implications in understanding the sequence of events in antigen processing and the correlation between antigen structure and immunodominance.

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Doyle, A., W. J. Martin, K. Funa, A. Gazdar, D. Carney, S. E. Martin, I. Linnoila, F. Cuttitta, J. Mulshine, and P. Bunn. "Markedly decreased expression of class I histocompatibility antigens, protein, and mRNA in human small-cell lung cancer." Journal of Experimental Medicine 161, no. 5 (May 1, 1985): 1135–51. http://dx.doi.org/10.1084/jem.161.5.1135.

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We have found markedly deficient expression of the class I major histocompatibility antigens HLA-A,B,C and beta 2m on human small-cell lung cancer (SCLC) lines and fresh tumor samples. The deficit of HLA-A,B,C and beta 2-microglobulin (beta 2m) antigen expression was demonstrated with both radiobinding assays and indirect immunofluorescence assays. Immunoprecipitation of metabolically labeled cells with antibodies to class I antigens showed most SCLC lines to have synthesized almost no beta 2m and HLA-A,B,C proteins. Northern blot analysis, using human HLA-A,B, and beta 2m cDNA probes, showed that almost all SCLC lines tested had markedly decreased amounts of HLA and beta 2m mRNA, but both gene products could be induced with interferon treatment of SCLC lines. We conclude that human SCLC, in contrast to other lung cancer types, is characterized by greatly reduced transcription of HLA-A,B,C and beta 2m genes, which suggests the existence of a mechanism for evading the host immune response to the tumor and of an E1a-like product in this type of tumor cell.

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Ogasawara, M., D. H. Kono, and D. T. Yu. "Mimicry of human histocompatibility HLA-B27 antigens by Klebsiella pneumoniae." Infection and Immunity 51, no. 3 (1986): 901–8. http://dx.doi.org/10.1128/iai.51.3.901-908.1986.

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Driianska, V., O. Petrina, M. Velychko, F. Haisenyuk, and G. Drannik. "Peculiarities of phenotypes of patients with pyelo- and glomerulonephritis by HLA distribution analysis." Ukrainian Journal of Nephrology and Dialysis, no. 4(60) (December 26, 2018): 11–18. http://dx.doi.org/10.31450/ukrjnd.4(60).2018.02.

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Studies devoted to the role of human leucocyte antigens (HLA) in pathogenesis of chronic kidney disease (CKD) have demonstrated the associative links of the HLA antigens, which stipulate the relative and attributive risks of some autoimmune diseases, with immune disorder and a high production of pro-inflammatory cytokines. The aim of our study was to determine the peculiarities of phenotypes of CKD patients according to the distribution of HLA-A, B and DR antigens and to conduct their comparative analysis in patients with pyelonephritis (PN) and glomerulonephritis (GN). Methods: The distribution of HLA-A, B, DR antigens in 384 CKD patients (120 with PN and 264 with GN) was analyzed. HLA antigens were defined using a standard microlymphocytotoxic test on the Terasakiґs planchette with special panels of anti-HLA serums (20 antigens of locus A, 31 – B and 9 – DR). The control group consisted of 350 healthy donors. The HLA antigen frequencies in normal and diseased subjects were compared taking each antigen separately, using χ2 test. The etiologic fraction (attributive risk s > 0,1) was counted using the formula: s = x - y/I- y, where x is frequency of antigen in patients and y is frequency in healthy. The s reading was considered reliable when it exceeded 0.1. Results. The causal role (σ > 0,1) was determined for А10, А11; В14, В16 for PN; antigens-protectors - А2, В21, В35, В40. For CGN, NS the relative risk is high (RR > 2) at the presence of HLA-A23, А24, А28; B8, В38, В41, В44; DR1, DR4, DRw52 in phenotype, the causal role in etiopathology (σ>0.1) is indicated for A24,А28; B8; DR1, DR4, DRw52; the disease protectors are B12 and B16. Conclusion. Conclusion. The features of the HLA-phenotype of patients with pyelo- and glomerulonephritis were shown. It allowed to establish the interconnectedness of the antigens of the histocompatibility complex with the risk of kidney diseases developing, which could help to personificate of the treatment and predicte of the course of the disease.

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Archbold, Julia K., Whitney A. Macdonald, Stephanie Gras, Lauren K. Ely, John J. Miles, Melissa J. Bell, Rebekah M. Brennan, et al. "Natural micropolymorphism in human leukocyte antigens provides a basis for genetic control of antigen recognition." Journal of Experimental Medicine 206, no. 1 (January 12, 2009): 209–19. http://dx.doi.org/10.1084/jem.20082136.

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Human leukocyte antigen (HLA) gene polymorphism plays a critical role in protective immunity, disease susceptibility, autoimmunity, and drug hypersensitivity, yet the basis of how HLA polymorphism influences T cell receptor (TCR) recognition is unclear. We examined how a natural micropolymorphism in HLA-B44, an important and large HLA allelic family, affected antigen recognition. T cell–mediated immunity to an Epstein-Barr virus determinant (EENLLDFVRF) is enhanced when HLA-B*4405 was the presenting allotype compared with HLA-B*4402 or HLA-B*4403, each of which differ by just one amino acid. The micropolymorphism in these HLA-B44 allotypes altered the mode of binding and dynamics of the bound viral epitope. The structure of the TCR–HLA-B*4405EENLLDFVRF complex revealed that peptide flexibility was a critical parameter in enabling preferential engagement with HLA-B*4405 in comparison to HLA-B*4402/03. Accordingly, major histocompatibility complex (MHC) polymorphism can alter the dynamics of the peptide-MHC landscape, resulting in fine-tuning of T cell responses between closely related allotypes.

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Posavec, Ana, and Renata Zunec. "Distribution of minor histocompatibility antigens HA-1, HA-2 and HA-8 in the Croatian population." Molecular and experimental biology in medicine 3, no. 1 (June 1, 2020): 29–33. http://dx.doi.org/10.33602/mebm.3.1.5.

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Minor histocompatibility antigens (mHAgs) are polymorphic, endogenously synthetized products recognized by alloreactive T cells in the context of major histocompatibility complex molecules. Recipients of allogeneic bone marrow grafts run the risk of graft-versus-host disease (GvHD), even when the donor is an HLA-identical sibling. This may be caused by disparities in mHAgs between the donor and the recipient, with the antigen present in the recipient and not in the donor. In such cases, T cells in the transplanted donor marrow respond to the recipient’s mHAgs. We determined the allele, genotype and phenotype frequencies for mHAgs HA-1, HA-2 and HA-8 in 102 healthy, unrelated individuals previously typed for HLA-A, HLA-B and HLA-DR. We compared the results with existing studies in other populations and found no significant differences between allele, genotype and phenotype frequencies in the Croatian population and frequencies reported for Caucasian population. The results presented will be used for further studies investigating the role of mHAgs in hematopoietic stem cell transplantation.

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Subklewe, Marion, Casper Paludan, Ming L. Tsang, Karsten Mahnke, Ralph M. Steinman, and Christian Münz. "Dendritic Cells Cross-Present Latency Gene Products from Epstein-Barr Virus–Transformed B Cells and Expand Tumor-Reactive Cd8+ Killer T Cells." Journal of Experimental Medicine 193, no. 3 (February 5, 2001): 405–12. http://dx.doi.org/10.1084/jem.193.3.405.

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Dendritic cells (DCs) are not targets for infection by the transforming Epstein-Barr virus (EBV). To test if the adjuvant role of DCs could be harnessed against EBV latency genes by cross-presentation, DCs were allowed to process either autologous or human histocompatibility leukocyte antigen (HLA)-mismatched, transformed, B lymphocyte cell lines (LCLs) that had been subject to apoptotic or necrotic cell death. After phagocytosis of small numbers of either type of dead LCL, which lacked direct immune-stimulatory capacity, DCs could expand CD8+ T cells capable of killing LCLs that were HLA matched to the DCs. Necrotic EBV-transformed, major histocompatibility complex (MHC) class I–negative LCLs, when presented by DCs, also could elicit responses to MHC class II–negative, EBV-transformed targets that were MHC class I matched to the DCs, confirming efficient cross-presentation of LCL antigens via MHC class I on the DC. Part of this EBV-specific CD8+ T cell response, in both lytic and interferon γ secretion assays, was specific for the EBV nuclear antigen (EBNA)3A and latent membrane protein (LMP)2 latency antigens that are known to be expressed at low levels in transformed cells. The induced CD8+ T cells recognized targets at low doses, 1–10 nM, of peptide. Therefore, the capacity of DCs to cross-present antigens from dead cells extends to the expansion of high affinity T cells specific for viral latency antigens involved in cell transformation.

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Luo, Heng, Hao Ye, Hui Wen Ng, Lemming Shi, Weida Tong, Donna L. Mendrick, and Huixiao Hong. "Machine Learning Methods for Predicting HLA-Peptide Binding Activity." Bioinformatics and Biology Insights 9s3 (January 2015): BBI.S29466. http://dx.doi.org/10.4137/bbi.s29466.

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As major histocompatibility complexes in humans, the human leukocyte antigens (HLAs) have important functions to present antigen peptides onto T-cell receptors for immunological recognition and responses. Interpreting and predicting HLA-peptide binding are important to study T-cell epitopes, immune reactions, and the mechanisms of adverse drug reactions. We review different types of machine learning methods and tools that have been used for HLA-peptide binding prediction. We also summarize the descriptors based on which the HLA-peptide binding prediction models have been constructed and discuss the limitation and challenges of the current methods. Lastly, we give a future perspective on the HLA-peptide binding prediction method based on network analysis.

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Mishra, Vikash Chandra, Dinesh Chandra, and Vimarsh Raina. "Histocompatibility Testing: A Fundamental Aspect of Renal Transplant Workup." Transplantology 5, no. 2 (May 15, 2024): 85–97. http://dx.doi.org/10.3390/transplantology5020009.

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Histocompatibility testing is pivotal in any renal transplantation workup, aimed at enhancing prospective donor recipient compatibility and improving transplant outcomes. The evolution and advancement of histocompatibility testing, particularly HLA typing, have significantly improved its precision. This study outlines the historical progression from serologic to DNA-based HLA typing, emphasizing the role of HLA proteins in immune response. Anti-HLA antibodies, targeting HLA proteins, pose challenges in renal transplantation. Monitoring and managing these antibodies are critical for renal transplant success. Complement-dependent cytotoxicity crossmatch and flow cytometry crossmatch are essential techniques for assessing donor–recipient compatibility. Panel-reactive antibody assesses antibodies against a panel of donor antigens, often HLA. Higher PRA levels (percentage) complicate donor matching, requiring specialized protocols. Virtual crossmatch evaluates recipient anti-HLA antibodies against potential donors through synthetic beads. This approach predicts crossmatch outcomes by comparing antibody profiles, offering a valuable tool for the risk assessment of renal transplantation. Despite advancements, a comprehensive understanding of alloreactive immune responses requires a combination of assays, emphasizing the importance of a multifaceted approach in histocompatibility testing. This is an attempt to compile the relevant information, providing a basis for comparison in a clear and foundational format for histocompatibility testing laboratories.

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Journal articles on the topic 'HLA histocompatibility antigens'

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