Статті в журналах: "HLA class II geners"

1

Hu, Renming, Carter Beck, Youn-Bok Chang, and Leslie J. Degroot. "HLA Class II Genes in Graves' Disease." Autoimmunity 12, no. 2 (January 1992): 103–6. http://dx.doi.org/10.3109/08916939209150316.

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2

Peterlin, B. Matija, Göran Andersson, Erika Lötscher, and Sue Tsang. "Transcriptional regulation of HLA class-II genes." Immunologic Research 9, no. 3 (September 1990): 164–77. http://dx.doi.org/10.1007/bf02918176.

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3

Sonneveld, Dirk J. A., Martijn F. Lutke Holzik, Ilja M. Nolte, Dirk Th Sleijfer, Winette T. A. van der Graaf, Marcel Bruinenberg, Rolf H. Sijmons, Harald J. Hoekstra, and Gerard J. Te Meerman. "Testicular carcinoma and HLA Class II genes." Cancer 95, no. 9 (October 25, 2002): 1857–63. http://dx.doi.org/10.1002/cncr.10903.

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4

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

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5

Silver, Jack. "Evolution of HLA class-II genes and haplotypes." Immunologic Research 9, no. 3 (September 1990): 212–22. http://dx.doi.org/10.1007/bf02918180.

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6

Piatier-Tonneau, D., P. Turmel, C. Auffray, and D. Charron. "Construction of chain- and locus-specific HLA class II DNA probes. Study of HLA-class II transcripts in leukemias." Journal of Immunology 137, no. 6 (September 15, 1986): 2050–56. http://dx.doi.org/10.4049/jimmunol.137.6.2050.

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Abstract In addition to their role in the immune response, MHC class II antigens may be considered as differentiation markers on hemopoietic cells. To study expression of class II genes at the mRNA level in leukemias representing various stages of lymphoid and myeloid differentiation, we constructed chain- and locus-specific HLA class II DNA probes. As the genes encoding the DR, DQ, and DP beta-chains display a strong sequence homology in the second extracellular and transmembrane domains, we used probes derived from the less conserved 3' untranslated regions. For the more divergent alpha-chain genes, DNA fragments derived from the coding portion were obtained from cDNA clones. All probes were designed to minimize background due to AT- or GC-rich segments and subcloned into pUC plasmids. Their lack of cross-hybridization was demonstrated in Southern blot experiments under moderately stringent conditions. Northern blot analysis of RNA from 15 patients with acute lymphoblastic and myeloblastic leukemias, chronic lymphoid and hairy cell leukemias showed that most patients expressed variable amounts of class II transcripts, some lacked all class II mRNA, and only two patients had a dissociated expression of class II genes, with lack of DQ and presence of DR and DP mRNA. This study reveals a vast heterogeneity of MHC class II gene expression in leukemias, as previously demonstrated at the protein level. The availability of these highly specific DNA probes should prove useful in extensive studies directed at better defining HLA class II gene expression during hemopoietic differentiation in physiologic and pathologic states.

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7

Douhan, John, Rebecca Lieberson, Joan H. M. Knoll, Hong Zhou, and Laurie H. Glimcher. "An Isotype-specific Activator of Major Histocompatibility Complex (MHC) Class II Genes That Is Independent of Class II Transactivator." Journal of Experimental Medicine 185, no. 11 (June 2, 1997): 1885–95. http://dx.doi.org/10.1084/jem.185.11.1885.

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Patients with one type of major histocompatibility complex class II combined immunodeficiency have mutations in a gene termed class II transactivator (CIITA), which coordinately controls the transcription of the three major human class II genes, HLA-DR, -DQ, and -DP. However, the experimentally derived B-lymphoblastoid cell line, clone 13, expresses high levels of HLADQ in the absence of HLA-DR and HLA-DP, despite its mapping by complementation analysis to this group. It was possible that one of the clone 13 CIITA alleles bore a mutation that allowed HLA-DQ, but not HLA-DR or -DP transcription. Alternatively, another factor, distinct from CIITA, might control HLA-DQ expression. We report here that ectopic expression of CIITA cDNAs derived by reverse transcriptase polymerase chain reaction from clone 13 do not restore expression of HLA-DQ in another CIITA-deficient cell line, RJ2.2.5. In addition, no CIITA protein is detectable in clone 13 nuclear extracts. In contrast, somatic cell fusion between clone 13 and RJ2.2.5 restored expression of the HLA-DQ haplotype encoded by the RJ2.2.5 DQB gene. Taken together, these data demonstrate the existence of an HLA-DQ isotype-specific trans-acting factor, which functions independently of CIITA.

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8

Westerheide, S. D., P. Louis-Plence, D. Ping, X. F. He, and J. M. Boss. "HLA-DMA and HLA-DMB gene expression functions through the conserved S-X-Y region." Journal of Immunology 158, no. 10 (May 15, 1997): 4812–21. http://dx.doi.org/10.4049/jimmunol.158.10.4812.

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Abstract The MHC class II homologous proteins HLA-DMA and HLA-DMB function in the loading of peptides onto class II molecules. Like the class II genes, the HLA-DM genes contain upstream regulatory sequences similar to the S-X-Y regulatory region as well as additional putative regulatory sites. To determine whether the DM genes are regulated in a similar manner as class II genes, a series of in vivo and in vitro analyses was performed. Deletion analysis showed that expression from the DM promoters is dependent on the conserved S-X-Y region. The class II-specific transcription factors RFX and CIITA are also required for expression, as cell lines deficient in these factors failed to allow transcription from the DM promoters. In addition, in vivo footprint analysis showed the putative X and Y boxes to be occupied by transcription factors in wild-type B cells, but not in RFX-deficient B cells. In astrocytes, IFN-gamma treatment induced increased occupancy of these sites. None of the other putative regulatory sites was occupied in vivo, indicating that they may not be functional. Finally, gel shift analysis showed synergistic complex formation between proteins that bind to the putative X boxes of the DM genes, as is found for the DRA gene. Therefore, the DM genes share a common mechanism of regulation with the class II genes.

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9

Ito, K., H. J. Bian, M. Molina, J. Han, J. Magram, E. Saar, C. Belunis, et al. "HLA-DR4-IE chimeric class II transgenic, murine class II-deficient mice are susceptible to experimental allergic encephalomyelitis." Journal of Experimental Medicine 183, no. 6 (June 1, 1996): 2635–44. http://dx.doi.org/10.1084/jem.183.6.2635.

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To investigate the development of HLA-DR-associated autoimmune diseases, we generated transgenic (Tg) mice with HLA-DRA-IE alpha and HLA-DRB1*0401-IE beta chimeric genes. The transgene-encoded proteins consisted of antigen-binding domains from HLA-DRA and HLA-DRB1*0401 molecules and the remaining domains from the IE(d)-alpha and IE(d)-beta chains. The chimeric molecules showed the same antigen-binding specificity as HLA-DRB1*0401 molecules, and were functional in presenting antigens to T cells. The Tg mice were backcrossed to MHC class II-deficient (IA beta-, IE alpha-) mice to eliminate any effect of endogenous MHC class II genes on the development of autoimmune diseases. As expected, IA alpha beta or IE alpha beta molecules were not expressed in Tg mice. Moreover, cell-surface expression of endogenous IE beta associated with HLA-DRA-IE alpha was not detectable in several Tg mouse lines by flow cytometric analysis. The HLA-DRA-IE alpha/HLA-DRB1*0401-IE beta molecules rescued the development of CD4+ T cells in MHC class II-deficient mice, but T cells expressing V beta 5, V beta 11, and V beta 12 were specifically deleted. Tg mice were immunized with peptides, myelin basic protein (MBP) 87-106 and proteolipid protein (PLP) 175-192, that are considered to be immunodominant epitopes in HLA-DR4 individuals. PLP175-192 provoked a strong proliferative response of lymph node T cells from Tg mice, and caused inflammatory lesions in white matter of the CNS and symptoms of experimental allergic encephalomyelitis (EAE). Immunization with MBP87-106 elicited a very weak proliferative T cell response and caused mild EAE. Non-Tg mice immunized with either PLP175-192 or MBP87-106 did not develop EAE. These results demonstrated that a human MHC class II binding site alone can confer susceptibility to an experimentally induced murine autoimmune disease.

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10

Chen, Yang-Yi, Wei-An Chang, En-Shyh Lin, Yi-Jen Chen, and Po-Lin Kuo. "Expressions of HLA Class II Genes in Cutaneous Melanoma Were Associated with Clinical Outcome: Bioinformatics Approaches and Systematic Analysis of Public Microarray and RNA-Seq Datasets." Diagnostics 9, no. 2 (June 12, 2019): 59. http://dx.doi.org/10.3390/diagnostics9020059.

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Major histocompatibility complex (MHC) class II molecules, encoded by human leukocyte antigen (HLA) class II genes, play important roles in antigen presentation and initiation of immune responses. However, the correlation between HLA class II gene expression level and patient survival and disease progression in cutaneous melanoma is still under investigation. In the present study, we analyzed microarray and RNA-Seq data of cutaneous melanoma from The Cancer Genome Atlas (TCGA) using different bioinformatics tools. Survival analysis revealed higher expression level of HLA class II genes in cutaneous melanoma, especially HLA-DP and -DR, was significantly associated with better overall survival. Furthermore, the expressions of HLA class II genes were most closely associated with survival in cutaneous melanoma as compared with other cancer types. The expression of HLA class II co-expressed genes, which were found to associate with antigen processing, immune response, and inflammatory response, was also positively associated with overall survival in cutaneous melanoma. Therefore, the results indicated that increased HLA class II expression may contribute to enhanced anti-tumor immunity and related inflammatory response via presenting tumor antigens to the immune system. The expression pattern of HLA class II genes may serve as a prognostic biomarker and therapeutic targets in cutaneous melanoma.

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11

Marsh, Steven G. E., and Julia G. Bodmer. "HLA class II nucleotide sequences, 1991." Human Immunology 31, no. 3 (January 1991): 207–27. http://dx.doi.org/10.1016/0198-8859(91)90027-7.

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12

Marsh, Steven G. E., and Julia G. Bodmer. "HLA class II nucleotide sequences, 1992." Human Immunology 35, no. 1 (September 1992): 1–17. http://dx.doi.org/10.1016/0198-8859(92)90090-a.

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13

Marsh, Steven G. E., and Julia G. Bodmer. "HLA Class II nucleotide sequences, 1991." Tissue Antigens 37, no. 4 (April 1991): 181–89. http://dx.doi.org/10.1111/j.1399-0039.1991.tb01870.x.

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14

Marsh, Steven G. E., and Julia G. Bodmer. "HLA Class II nucleotide sequences, 1992." Tissue Antigens 40, no. 5 (November 1992): 229–43. http://dx.doi.org/10.1111/j.1399-0039.1992.tb02050.x.

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15

Zhou, H., H. S. Su, X. Zhang, J. Douhan, and L. H. Glimcher. "CIITA-dependent and -independent class II MHC expression revealed by a dominant negative mutant." Journal of Immunology 158, no. 10 (May 15, 1997): 4741–49. http://dx.doi.org/10.4049/jimmunol.158.10.4741.

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Abstract The MHC class II transactivator gene (CIITA) coordinately controls the expression of the three major human class II genes, HLA-DR, HLA-DQ, and HLA-DP. Indeed, patients with one form of MHC class II immunodeficiency disease, due to defective CIITA genes, lack expression of all three isotypes. Nevertheless, there is substantial evidence that human class II genes are not always coordinately regulated, raising the possibility that CIITA-independent, isotype-specific class II regulatory pathways exist. To address this issue, we have generated a dominant negative mutant of CIITA that lacks the acidic transcription-activating N terminus, but retains the proline/serine/threonine-rich domain. Three newly produced anti-CIITA mAbs revealed that this mutant protein lacked N-terminal epitopes. In this study, we report that this CIITA dominant negative mutant repressed the constitutive expression of all three class II isotypes in human EBV-B cell lines, as well as IFN-gamma-induced class II transcription in HeLa cells. However, in a CIITA-deficient, EBV-transformed B cell line, clone 13, the dominant negative mutant did not alter the endogenous expression of the HLA-DQ gene. Taken together, these data demonstrate the existence of both CIITA-dependent and -independent class II regulatory pathways. Furthermore, our data provide evidence that the latter pathways can be isotype specific.

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16

AMAR, AVRAHAM, SUSAN L. HOLBECK, and GERALD T. NEPOM. "SPECIFIC ALLELIC VARIATION AMONG LINKED HLA CLASS II GENES." Transplantation 44, no. 6 (December 1987): 831–35. http://dx.doi.org/10.1097/00007890-198712000-00022.

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17

MÖLLER, ERNA, B. CARLSSON, O. OLERUP, and J. WALLIN. "Polymorphism of HLA Class II Genes in Various Diseases." Annals of the New York Academy of Sciences 546, no. 1 Molecular Bas (December 1988): 143–50. http://dx.doi.org/10.1111/j.1749-6632.1988.tb21629.x.

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18

SORIANO, JOAN B, GUADALUPE ERCILLA, JORDI SUNYER, FRANCISCO X REAL, CONXI LÁZARO, MARÍA J RODRIGO, XAVIER ESTIVILL, et al. "HLA Class II Genes in Soybean Epidemic Asthma Patients." American Journal of Respiratory and Critical Care Medicine 156, no. 5 (November 1997): 1394–98. http://dx.doi.org/10.1164/ajrccm.156.5.9701064.

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19

Bidwell, Jeffrey L., Elizabeth A. Bidwell, and Benjamin A. Bradley. "8 HLA Class II genes: typing by DNA analysis." Baillière's Clinical Haematology 3, no. 2 (April 1990): 355–84. http://dx.doi.org/10.1016/s0950-3536(05)80055-1.

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20

Castro, R., H. Yang, R. Apple, S. Targan, H. A. Erlich, and J. I. Rotter. "Inflammatory bowel disease associations with HLA-class II genes." Human Immunology 40 (January 1994): 95. http://dx.doi.org/10.1016/0198-8859(94)91847-3.

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21

Levine, F., H. A. Erlich, B. Mach, and D. Pious. "Transcriptional regulation of HLA class II and invariant chain genes." Journal of Immunology 134, no. 1 (January 1, 1985): 637–40. http://dx.doi.org/10.4049/jimmunol.134.1.637.

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Abstract Class II (Ia) antigens are coded for by a family of genes located in the human MHC (HLA). These genes are regulated in a complex manner, being constitutively expressed, inducibly expressed, or not expressed, depending on the cell type examined. 6.1.6 is a variant of a normal B lymphoblastoid line that has lost expression of all class II molecules and has previously been shown to have a defect in the regulation of class II genes. In this report, we have examined those genes by Southern and Northern blotting and have found that 6.1.6 is severely deficient in mRNA for all class II genes examined, although the genes are structurally intact. P30, a partial revertant of 6.1.6, re-expresses mRNA for a subset of class II genes. mRNA for the class II-associated invariant chain is substantially reduced but not absent in 6.1.6.

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22

Sillé, F. C. M., L. Conde, J. Zhang, N. K. Akers, S. Sanchez, J. Maltbaek, J. E. Riby, M. T. Smith, and C. F. Skibola. "Follicular lymphoma-protective HLA class II variants correlate with increased HLA-DQB1 protein expression." Genes & Immunity 15, no. 2 (December 5, 2013): 133–36. http://dx.doi.org/10.1038/gene.2013.64.

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23

Thonnard, J., F. Deldime, M. Heusterspreute, B. Delepaut, F. Hanon, M. De Bruyère, and M. Philippe. "HLA class II genotyping: two assay systems compared." Clinical Chemistry 41, no. 4 (April 1, 1995): 553–56. http://dx.doi.org/10.1093/clinchem/41.4.553.

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Abstract In the last few years, a variety of DNA-based human leukocyte antigen (HLA) typing methods have emerged, revealing the extreme polymorphism of HLA genes. This polymorphism makes it difficult for a clinical laboratory to establish the best HLA typing strategy. In this study we have compared two techniques for performing HLA-DRB typing: a commercial rapid assay based on the polymerase chain reaction (PCR) followed by reverse dot-blot hybridization of the PCR products (the Inno-LiPA assay), and a method based on PCR followed by restriction fragment length polymorphism analysis. We found that both methods provide reliable results with a high rate of concordance (97%) and that Inno-LiPA is convenient for large-scale routine typing. However, if a high-resolution allelic typing is required, each method lacks accuracy but using them in association improves the accuracy of the results.

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24

Hagihara, Masao, Tatsuo Shimura, Kozue Yamamoto, Kentaro Takebe, Batmunkh Munkhbat, and Kimiyoshi Tsuji. "Soluble HLA class I and class II in Japanese." Human Immunology 40, no. 3 (July 1994): 171–73. http://dx.doi.org/10.1016/0198-8859(94)90064-7.

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25

Poluektov, Yuri, AeRyon Kim, Stanislav Khoruzhenko, and Scheherazade Sadegh-Nasseri. "The effects of HLA-DO on peptide binding by MHC Class II HLA-DR1 (130.14)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 130.14. http://dx.doi.org/10.4049/jimmunol.184.supp.130.14.

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Abstract Ever since the discovery of the HLA-DOA and HLA-DOB genes in the HLA Class II region, controversy has surrounded their true function. Studies resulting in transcriptional modification of the HLA-DO gene analogs in mice (H-2O) support the general theory that DO decreases the presentation of antigens through the MHC class II system by inhibiting the effects of the MHC class II accessory molecule HLA-DM. The mechanism of such inhibition, however, still remains a mystery. To shed some light on this issue, we have constructed a recombinant form of soluble HLA-DO, without its cytoplasmic anchors, and conducted peptide binding experiments with soluble forms of recombinant HLA-DM and HLA-DR1. Our experiments indicate that DO can have both a negative and a positive effect on peptide presentation by the MHC Class II molecule HLA-DR1, depending on the quality of the anchoring residues of the peptide. In addition, HLA-DO only affects peptide association to the MHC Class II molecules and has virtually no effect on peptide dissociation.

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26

Pious, D., L. Dixon, F. Levine, T. Cotner, and R. Johnson. "HLA class II regulation and structure. Analysis with HLA-DR3 and HLA-DP point mutants." Journal of Experimental Medicine 162, no. 4 (October 1, 1985): 1193–207. http://dx.doi.org/10.1084/jem.162.4.1193.

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Point mutations that affect HLA-DR structure or expression have not previously been described. In the present study, we isolated such mutants by immunoselection of an ethyl methanesulfonate-mutagenized HLA-DR3 cell line with an anti-HLA-DR3 monoclonal antibody, 16.23. To facilitate analysis, we used a parent cell line with a preexisting deletion of one haplotype encompassing DR and DQ alpha and beta. The selection yielded two sets of mutants, one with defects in DR3 structure, the other with defects in different steps leading to DR expression. Of the expression-defective mutants, one had undergone a second deletion removing the remaining DR alpha gene but no other class II genes. It had a normal abundance of DR beta mRNA but had lost binding of DR monomorphic antibodies, indicating that DR beta chains do not form noncognate dimers. A second mutant had an abnormally large DR alpha mRNA, probably resulting from a splice site mutation. Several mutants had marked reductions in DR beta mRNA levels; in two of these, the lesion appeared to be transcriptional because the reduction in DR beta mRNA was paralleled by an altered methylation pattern of one of the DR beta genes. Other expression-defective mutants had different posttranscriptional defects. Some of the mutations were similar to those that have been found in mouse strains defective in I-E expression, whereas others have no known natural counterpart. The matrix of reactivities of anti-HLA class II monomorphic antibodies with these and similar mutants allowed us to define the gene products recognized by these antibodies. A set of seven mutants were "epitope defective," that is, they expressed normal or near normal levels of HLA-DR3 but no longer bound 16.23. Unexpectedly, each of the epitope mutants had decreased DR dimer stability. These mutants should be useful in localizing the DR3 alloepitope and in elucidating its contribution as a restriction element in the presentation of soluble antigen to immune T cells.

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27

Nagler, Adi, Shelly Kalaora, Chaya Barbolin, Anastasia Gangaev, Steven L. C. Ketelaars, Michal Alon, Joy Pai, et al. "Identification of presented SARS-CoV-2 HLA class I and HLA class II peptides using HLA peptidomics." Cell Reports 35, no. 13 (June 2021): 109305. http://dx.doi.org/10.1016/j.celrep.2021.109305.

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28

Tilanus, M. G. J., M. C. J. A. van Eggermond, M. van der Bijl, B. Morolli, G. M. Th Schreuder, R. R. P. De Vries, and M. J. Giphart. "HLA class II DNA analysis by RFLP reveals novel class II polymorphism." Human Immunology 18, no. 4 (April 1987): 265–76. http://dx.doi.org/10.1016/0198-8859(87)90074-7.

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29

Amaldi, I., W. Reith, C. Berte, and B. Mach. "Induction of HLA class II genes by IFN-gamma is transcriptional and requires a trans-acting protein." Journal of Immunology 142, no. 3 (February 1, 1989): 999–1004. http://dx.doi.org/10.4049/jimmunol.142.3.999.

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Abstract HLA class II Ag are encoded by a family of related genes clustered in the HLA-D region of the MHC. The expression of this multi-gene family is highly regulated and this regulation is essential for the control of the immune response. Class II gene expression is constitutive in a limited number of cell types and can be induced by IFN-gamma in a number of class II negative cells. In this study, we have clarified two essential aspects of the regulation of HLA class II genes by IFN-gamma. 1) The induction mechanism operates at the level of transcription and there is a long lag phase in the signal transduction process. 2) The induction of class II genes requires the de novo synthesis of a new protein(s). On this basis, we propose that IFN-gamma regulates the transcription of HLA class II genes via the de novo synthesis of a trans-acting activator protein.

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30

Leclerc, Michel, and Loïc Baerlocher. "Mapping on Sea-Star MHC Genes in Invertebrates." European Journal of Biology and Biotechnology 2, no. 2 (April 6, 2021): 60–62. http://dx.doi.org/10.24018/ejbio.2021.2.2.170.

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MHC genes have been discovered in Echinodermata (Invertebrates containing 5 classes).2 classes (Ophuirids, Crinoïds) out of 5 possess HLA E, HLA B (Class I), HLADRB1, HLADQB1 (Class II). By the use of Mapping we identified 2 other MHC genes (Class II) in another Echinodermata: the sea star Asterias rubens (Asterids).

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31

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

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

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32

SIMEÓN, CARMEN P., VICENT FONOLLOSA, CARLES TOLOSA, EDUARD PALOU, ALBERT SELVA, ROSER SOLANS, LLUIS ARMADANS, ESTEFANIA MORENO, SARA MARSAL, and MIQUEL VILARDELL. "Association of HLA Class II Genes with Systemic Sclerosis in Spanish Patients." Journal of Rheumatology 36, no. 12 (November 2, 2009): 2733–36. http://dx.doi.org/10.3899/jrheum.090377.

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Objective.To examine the role of HLA-DRB1 and HLA-DQB1 alleles in the susceptibility to systemic sclerosis (SSc) and its clinical expression in a Spanish population.Methods.One hundred Spanish Caucasian patients with SSc and 130 controls were studied. Molecular HLA-DRB1 and HLA-DQB1 typing was performed by polymerase chain reaction (PCR) sequence-based typing and PCR sequence-specific oligonucleotide.Results.HLA-DRB1*11 was associated with genetic susceptibility to SSc, whereas HLA-DRB1*07 (HLA-DRB1*0701) showed a protective effect. A significant increase in the frequency of the DRB1*1104 allele was observed in patients with anti-topoisomerase I autoantibodies (anti-Topo I) while HLA-DRB1*01 and HLA-DQB1*05 alleles were significantly increased in patients with anti-centromere antibodies (ACA). The HLA-DRB1*11 allele was more frequent in patients with pulmonary fibrosis; however, no significant association with any HLA-DRB1 or DQB1 alleles was identified in patients with pulmonary arterial hypertension.Conclusion.HLA alleles play a role in genetic susceptibility to SSc in Spanish patients. Some alleles are more prevalent in patients with pulmonary fibrosis and in patients with certain SSc-specific autoantibodies (anti-Topo I and ACA).

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33

Noreen, H. J., M. L. Davidson, M. B. Stewart, and M. Segall. "RFLP analysis fo HLA class II phenotyping." Human Immunology 23, no. 2 (January 1988): 128. http://dx.doi.org/10.1016/0198-8859(88)90218-2.

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34

Vanderborght, Patricia R., Antonio G. Pacheco, Matilde Romero, Jose Roberto Moraes, Euzenir N. Sarno, Maria Elisa Moraes, and Milton O. Moraes. "HLA class II in infectious disease models." Human Immunology 66, no. 8 (August 2005): 123. http://dx.doi.org/10.1016/j.humimm.2005.08.233.

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35

Termijtelen, Annemarie. "T-cell allorecognition of HLA class II." Human Immunology 28, no. 1 (May 1990): 1–10. http://dx.doi.org/10.1016/0198-8859(90)90097-9.

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Londei, M., B. Grubeck-Loebenstein, M. Kissonerghis, P. Austin, J. Trowsdale, C. Greenall, and M. Feldmann. "Thyrocytes can synthesize HLA class II molecules." Acta Endocrinologica 116, no. 1_Suppl (August 1987): S82—S85. http://dx.doi.org/10.1530/acta.0.114s082.

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37

Gebe, J. A., E. Swanson, and W. W. Kwok. "HLA Class II peptide-binding and autoimmunity." Tissue Antigens 59, no. 2 (February 2002): 78–87. http://dx.doi.org/10.1034/j.1399-0039.2002.590202.x.

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38

Hmida, S., A. Gauthier, A. Dridi, F. Quillivic, B. Genetet, K. Boukef, and G. Semana. "HLA class II gene polymorphism in Tunisians." Tissue Antigens 45, no. 1 (January 1995): 63–68. http://dx.doi.org/10.1111/j.1399-0039.1995.tb02416.x.

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39

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

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40

MÜLLER, N., A. LOEBENFELDER, A. LORENZ, R. WANK, and M. ACKENHEIL. "HLA Class II Antigens in Endogenous Psychoses." Annals of the New York Academy of Sciences 650, no. 1 Ontogenetic a (April 1992): 322–25. http://dx.doi.org/10.1111/j.1749-6632.1992.tb49145.x.

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41

Fogdell-Hahn, A., A. Ligers, M. Grønning, J. Hillert, and O. Olerup. "Multiple sclerosis: a modifying influence of HLA class I genes in an HLA class II associated autoimmune disease." Tissue Antigens 55, no. 2 (February 2000): 140–48. http://dx.doi.org/10.1034/j.1399-0039.2000.550205.x.

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42

Concha, E. G., M. Fernandez-Arquero, J. L. Mendoza, L. Conejero, M. A. Figueredo, J. Perez Sema, M. Diaz-Rubio, and A. Ruiz Leon. "Contribution of HLA class II genes to susceptibility in achalasia." Tissue Antigens 52, no. 4 (October 1998): 381–84. http://dx.doi.org/10.1111/j.1399-0039.1998.tb03059.x.

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43

VALDES, A. M., S. K. McWEENEY, D. MEYER, M. P. NELSON, and G. THOMSON. "Locus and population specific evolution in HLA class II genes." Annals of Human Genetics 63, no. 1 (January 1999): 27–43. http://dx.doi.org/10.1046/j.1469-1809.1999.6310027.x.

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44

Mack, Douglas G., Jennifer J. Johnson, Fiona Roberts, Craig W. Roberts, Randee G. Estes, Chella David, F. Carl Grumet, and Rima McLeod. "HLA-class II genes modify outcome of Toxoplasma gondii infection." International Journal for Parasitology 29, no. 9 (September 1999): 1351–58. http://dx.doi.org/10.1016/s0020-7519(99)00152-6.

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45

Fujimoto, T., M. Sada, T. Nakano, K. Takeuchi, K. Horinouchi, T. Tsuji, and H. Akimoto. "Analysis of HLA class II genes of schizophrenia in Japanese." Human Immunology 47, no. 1-2 (April 1996): 38. http://dx.doi.org/10.1016/0198-8859(96)84889-0.

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46

Schenck, Carlos H., Edgar Garcia-Rill, Miriam Segall, Harriet Noreen, and Mark W. Mahowald. "HLA Class II genes associated with REM sleep behavior disorder." Annals of Neurology 39, no. 2 (February 1996): 261–63. http://dx.doi.org/10.1002/ana.410390216.

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47

Bertolaccini, M. L., T. Atsumi, A. R. Caliz, O. Amengual, M. A. Khamashta, G. R. V. Hughes, and T. Koike. "Association of antiphosphatidylserine/prothrombin autoantibodies with HLA class II genes." Arthritis & Rheumatism 43, no. 3 (March 2000): 683. http://dx.doi.org/10.1002/1529-0131(200003)43:3<683::aid-anr26>3.0.co;2-2.

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48

Haegert, D. G., M. Michaud, C. Schwab, and G. S. Francis. "Multiple sclerosis and HLA class II susceptibility and resistance genes." Journal of Neuroscience Research 26, no. 1 (May 1990): 66–73. http://dx.doi.org/10.1002/jnr.490260108.

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49

Siegler, Benedikt Hermann, Marc Altvater, Jan Niklas Thon, Christopher Neuhaus, Christoph Arens, Florian Uhle, Christoph Lichtenstern, Markus Alexander Weigand, and Sebastian Weiterer. "Postoperative abdominal sepsis induces selective and persistent changes in CTCF binding within the MHC-II region of human monocytes." PLOS ONE 16, no. 5 (May 3, 2021): e0250818. http://dx.doi.org/10.1371/journal.pone.0250818.

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Background Postoperative abdominal infections belong to the most common triggers of sepsis and septic shock in intensive care units worldwide. While monocytes play a central role in mediating the initial host response to infections, sepsis-induced immune dysregulation is characterized by a defective antigen presentation to T-cells via loss of Major Histocompatibility Complex Class II DR (HLA-DR) surface expression. Here, we hypothesized a sepsis-induced differential occupancy of the CCCTC-Binding Factor (CTCF), an architectural protein and superordinate regulator of transcription, inside the Major Histocompatibility Complex Class II (MHC-II) region in patients with postoperative sepsis, contributing to an altered monocytic transcriptional response during critical illness. Results Compared to a matched surgical control cohort, postoperative sepsis was associated with selective and enduring increase in CTCF binding within the MHC-II. In detail, increased CTCF binding was detected at four sites adjacent to classical HLA class II genes coding for proteins expressed on monocyte surface. Gene expression analysis revealed a sepsis-associated decreased transcription of (i) the classical HLA genes HLA-DRA, HLA-DRB1, HLA-DPA1 and HLA-DPB1 and (ii) the gene of the MHC-II master regulator, CIITA (Class II Major Histocompatibility Complex Transactivator). Increased CTCF binding persisted in all sepsis patients, while transcriptional recovery CIITA was exclusively found in long-term survivors. Conclusion Our experiments demonstrate differential and persisting alterations of CTCF occupancy within the MHC-II, accompanied by selective changes in the expression of spatially related HLA class II genes, indicating an important role of CTCF in modulating the transcriptional response of immunocompromised human monocytes during critical illness.

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Salter, R. D., J. Alexander, F. Levine, D. Pious, and P. Cresswell. "Evidence for two trans-acting genes regulating HLA class II antigen expression." Journal of Immunology 135, no. 6 (December 1, 1985): 4235–38. http://dx.doi.org/10.4049/jimmunol.135.6.4235.

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Abstract Previous studies have shown that a trans-acting regulatory factor is required for expression of HLA class II molecules in B-LCL, and that a trans-active factor derived from B-LCL induces de novo synthesis of T-LCL-encoded class II antigens in hybrids of T-LCL and B-LCL. To further examine the genetics of class II antigen regulation, we have now fused two different T-LCL with the class II antigen negative B-LCL 6.1.6, a regulatory mutant that does not synthesize a trans-acting factor necessary for transcription of class II genes. Northern blot analysis and cell surface immunofluorescence studies indicate that the hybrids express class II antigens encoded by both 6.1.6 and T-LCL parent cell lines. Thus, expression of class II antigens in these hybrids is controlled by a minimum of two trans-acting regulatory genes. One of these genes is inactivated in the 6.1.6 mutant and is provided by the T-LCL fusion partner. The second regulatory gene may still be active in 6.1.6, but it alone is insufficient for maintenance of class II antigen expression.

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