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Добірка наукової літератури з теми "HLA class II geners"

Автор: Grafiati
Опубліковано: 10 грудня 2022
Оновлено: 28 січня 2023

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Статті в журналах з теми "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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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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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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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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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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Дисертації з теми "HLA class II geners"

1

Sukiennicki, Teresa Lyn. "Regulation of expression of the HLA class II gene, DQB1 /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/8358.

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2

Wu, Zhonglin. "Molecular analysis of HLA class II genes : from Hashimoto's thyroiditis to thyrocytes." Thesis, Queen Mary, University of London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265188.

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3

Jonson, Carl-Oscar. "The Importance of CTLA-4 and HLA Class II for Type 1 Diabetes Immunology." Doctoral thesis, Linköping : Univ, 2007. http://www.bibl.liu.se/liupubl/disp/disp2007/med1020s.pdf.

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4

Gil, Julio Miranda. "Estudo da associação entre os alelos DR e DQ de antígenos de histocompatibilidade leucocitária (HLA) e pênfigo vulgar em pacientes brasileiros." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/5/5143/tde-10012017-105831/.

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INTRODUÇÃO: Pênfigo Vulgar é uma doença bolhosa mucocutânea autoimune caracterizada pela formação de bolhas ou ulcerações dolorosas que afetam as superfícies cutâneas e/ou mucosas. A perda do contato célulacélula entre os queratinócitos do epitélio (acantólise) resulta na manifestação clínica do Pênfigo Vulgar. Autoanticorpos IgG se ligam às desmogleínas - anti-desmogleína 3 (Dsg3) e/ou anti-desmogleína 1 (Dsg1) -e são críticos na patogênese da doença. A predisposição genética ao PV, principalmente com alelos HLA DR e DQ, foi revelada desde a década de 80 e foi comprovada por análises genéticas e sorológicas, repetidas vezes. As características singulares da população brasileira favorecem estudos genéticos exploratórios. PACIENTES E MÉTODO: O grupo em estudo incluiu 51 pacientes com diagnóstico confirmado de Pênfigo Vulgar de um hospital terciário da cidade de São Paulo, estado de São Paulo, sudeste do Brasil. Foi realizada a extração de DNA e a tipificação de HLA A, B, C, DR e DQ por meio de kits QIagen (QIAamp DNA Mini Kit®). O grupo controle foi composto a partir de um banco de dados de 297 doadores falecidos não relacionados da cidade de São Paulo, que foram tipados pelo mesmo método. Este banco faz parte do Sistema Estadual de Transplantes da Secretaria de Saúde do Governo do Estado de São Paulo e contém a idade do paciente na coleta. O nível de significância dos testes estatísticos foi ajustado pela correção de Bonferroni, dependendo da quantidade de frequências fenotípicas avaliadas para o HLA A, HLA B, HLA C, HLA DRB1 e HLA DQB1. RESULTADOS: Os alelos HLAB* 57, HLA-C*15, HLA-DRB1*04:02, HLA-DRB1*08:04, HLA-DRB1*14:01, DQA1*03:01, DQB1*03:02 e o DQB1*05:03 estiveram associados com a susceptibilidade. Ambos os alelos HLA DRB1*04:02 e HLA-DRB1*14:01 e seus respectivos haplótipos DRB1*04-DQA1*03:01-DQB1*03:02 e DRB1*14- DQA1*01:01-DQB1*05:03 conferiram risco à doença. DISCUSSÃO: Os alelos DRB1*04:02 e DQB1*05:03 estão associados com o Pênfigo Vulgar no presente estudo, bem como a diversas populações do mundo. A associação aqui estudada com o DRB1*08:04 foi confirmada por causa deste alelo específico e não do desequilíbrio de ligação a algum gene adjacente. A associação do alelo HLA-B*57 ao pênfigo vulgar é reportada pela primeira vez pelo presente estudo. CONCLUSÕES: Os alelos HLA-B*57, HLA-C*15, HLADRB1* 04:02, HLA-DRB1*08:04, HLA-DRB1*14:01, DQA1*03:01, DQB1*03:02 e DQB1*05:03 estão associados ao Pênfigo Vulgar em pacientes brasileiros
BACKGROUND: Pemphigus vulgaris is a mucocutaneous blistering autoimune disease that manifests as painful blisters or ulcerations on the skin and/or mucosal surfaces. The loss of cell-cell adhesion among the epithelial keratinocytes (acantholisis) leads to pemphigus vulgaris clinical findings. IgG autoantibodies target desmoglein - anti-Desmoglein 3 (Dsg3) and/or 1 (Dsg1) - play a major role in the disease pathogenesis. Genetic predisposal to pemphigus vulgaris, especially the HLA DR and DQ alleles, was revealed since the 80s and has been proven through genetic and serologic analysis repeatedly. The unique constitution of the Brazilian population favours genetics exploratory studies. PATIENTS AND METHODS: The study group included fifty-one patients with confirmed diagnosis of Pemphigus Vulgaris from a tertiary hospital in Sao Paulo\'s city and state, southeast Brazil. DNA extraction and HLA A, B, C, DR and DQ typing using Qiagen kits (QIAamp DNA Mini Kit®). The control group was composed by a database of 297 unrelated deceased donors from the city of São Paulo that were typed through the same method. This database is a part of the Transplants State System of the Government\'s Health Secretary from the State of Sao Paulo. The statistical significance level was adjusted by using the Bonferroni correction depending on the phenotypic frequencies evaluated to HLA A, HLA B, HLA C, HLA DRB1 e HLA DQB1. RESULTS: The alleles HLA-B*57, HLA-C*15, HLADRB1* 04:02, HLA-DRB1*08:04, HLA-DRB1*14:01, DQA1*03:01, DQB1*03:02 and DQB1*05:03 were associated with susceptibility. Both alleles HLA DRB1*04:02 and HLA-DRB1*14:01 and their respective haplotypes DRB1*04-DQA1*03:01-DQB1*03:02 and DRB1*14-DQA1*01:01-DQB1*05:03 conferred risk to the disease. DISCUSSION: The DRB1*04:02 and DQB1*05:03 alleles are associated with Pemphigus Vulgaris in our study, as well in various populations. The association in our study with HLA-DRB1*08:04 was confirmed to be specific to this allele and not to linkage disequilibrium to any adjacent gene. The association between HLA-B*57 and pemphigus vulgaris is being reported for the first time at the present study. CONCLUSIONS: The alleles HLA-B*57, HLA-C*15, HLA-DRB1*04:02, HLADRB1* 08:04, HLA-DRB1*14:01, DQA1*03:01, DQB1*03:02 and DQB1*05:03 were associated with Pemphigus Vulgaris in Brazilian patients
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Weber, Raimar. "Estudo da associação entre antígenos de histocompatibilidade leucocitária (HLA) e pênfigo vulgar em pacientes brasileiros." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/5/5143/tde-21122010-111128/.

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INTRODUÇÃO: O Pênfigo Vulgar é uma doença bolhosa crônica que acomente pele e mucosas. A perda de adesão epitelial ocorre por agressão autoimune às desmogleínas presentes nos desmossomos, mediada por anticorpos IgG. Estudos sobre a gênese da autoimunidade no pênfigo indicam associação entre alelos do sistema HLA, especialmente dos loci DR e DQ. A população brasileira apresenta características favoráveis a estudos exploratórios em genética decorrente de sua origem mista e intensa miscigenação. PACIENTES E MÉTODO: O grupo em estudo incluiu trinta e seis pacientes não consanguíneos com diagnóstico de Pênfigo Vulgar comprovado por imunopatologia provenientes do estado de São Paulo, Brasil. Foram tipados para os loci HLA-A, HLA-B e HLA-DR utilizando-se oligonucleotídeos sequência-específica (PCR-SSO). As frequências alélicas e fenotípicas encontradas foram comparadas com as de um grupo controle composto de dados de 712 indivíduos doadores voluntários cadastrados no Registro Nacional de Doadores de Medula Óssea (REDOME) provenientes de São Paulo e tipados pelo mesmo método. O valor de P crítico foi corrigido utilizando-se o método False Discovery Rate. RESULTADOS: Os alelos HLA-DRB1*04:02, DRB1*08:04 e DRB1*14 estiveram associados à doença com riscos relativos de 44,6, 18,6 e 4,8, respectivamente (p<0,001). Não houve diferença estatisticamente significante entre as frequências de nenhum alelo dos loci HLA-A ou HLA-B entre os grupos. DISCUSSÃO: O alelo DRB1*04:02, diretamente, e o alelo DRB1*14, indiretamente por desequilíbrio de ligação com DQB1*05:03, estão associados com Pênfigo Vulgar em diversas populações ao redor do mundo, porém nenhum estudo semelhante observou associação com o alelo DRB1*08:04 em tamanha magnitude. Acreditamos que as associações encontradas em nosso estudo não sejam decorrentes de viés de estratificação populacional. É necessária, no entanto, a tipagem de loci adjascentes ao HLA-DR dos indivíduos do grupo em estudo para diferenciar se o risco à doença é inerente a estes alelos ou a algum outro nas proximidades, com o qual estariam em desequilíbrio de ligação. CONCLUSÕES: Os alelos HLA-DRB1*04:02, DRB1*08:04 e DRB1*14 estiveram associados ao Pênfigo Vulgar em pacientes brasileiros.
BACKGROUND: Pemphigus vulgaris is a chronic blistering disease affecting skin and mucous membranes. Autoimmune aggression to desmoglein in desmosomes, mediated by IgG antibodies, leads to loss of epithelial cell adhesion. Studies indicate association between some alleles of the HLA system and pemphigus vulgaris, mainly at the DR and DQ loci. Brazilian population characteristics are conducive to genetic exploratory studies because of its various origins and intense ethnically admixture. PATIENTS AND METHODS: The study group consisted of thirty-six unrelated patients with clinical and immunopathological diagnosis of pemphigus vulgaris from a tertiary hospital in Sao Paulo - Brazil. HLA allele typing at the A, B and DR loci was performed after DNA extraction using polymerase chain reaction and sequence-specific oligonucleotide probes (PCR-SSO). Allele and phenotypic frequencies were compared to those from a control group composed by 712 individuals volunteer donors registered in a national registry of bone marrow donors (REDOME) from Sao Paulo, typed using the same method. False Discovery Rate method was used to adjust level of critical P values. RESULTS: The HLADRB1* 04:02, DRB1*08:04 and DRB1*14 were associated with pemphigus vulgaris with relative risks of 44.6, 18.6 and 4.8, respectively (p <0.001). There was no significant difference between the frequencies of any allele of loci HLAA or HLA-B among the groups. DISCUSSION: The alleles DRB1*04:02 and DRB1*14 (indirectly through linkage disequilibrium with the DQB1*05:03) are associated with pemphigus vulgaris in several populations worldwide, however, no similar study reported such magnitude of association between pemphigus vulgaris and DRB1*08:04 allele. We consider that the association is not secondary to population stratification bias. HLA typing of nearby loci is required to differentiate if the association with pemphigus vulgaris is inherent to the HLA-DRB1*08:04 allele or to another gene which is in linkage disequilibrium. CONCLUSIONS: The HLA-DRB1*04:02, DRB1*08:04 and DRB1*14 were associated with pemphigus vulgaris in Brazilian patients
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6

Silva, Milton Thiago Guerino da. "Avaliação de potencial agente vacinal contra o S.pyogenes em camundongos transgênicos, portadores de genes HLA de classe II humanos." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/5/5146/tde-20122011-155537/.

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A faringite estreptocócica desencadeada pelo Streptococcus pyogenes pode resultar em uma série de doenças humanas e complicações como a febre reumática (FR) em indivíduos predispostos não tratados. A FR é uma doença autoimune que afeta mais de 20 milhões de crianças em países em desenvolvimento. A proteína M presente na membrana do S. pyogenes representa o maior fator de virulência da bactéria, e é objetivo de estudos para o desenvolvimento de uma vacina contra essa patologia. Atualmente mais de 200 tipos de proteínas M foram descritos na literatura e a sua porção Cterminal é conservada entre os diferentes tipos. Desenvolvemos um protótipo de vacina que compreende 55 resíduos de aminoácido da porção C-terminal, denominado StreptInCor. Neste trabalho analisamos a resposta humoral e celular específica contra o peptídeo sintético StreptInCor, usando camundongos transgênicos portadores de HLA de classe II humanos DR2, DR4, DQ6 e DQ8. O protocolo de imunização consistiu em administrar 50 g do StreptInCor adsorvido em 300 g de hidróxido de alumínio nos dias 0 e 14. Os grupos controles foram injetados com salina nas mesmas condições. O soro obtido no 28º dia foi testado por ensaio imunoenzimático (ELISA) para verificarmos a presença de anticorpos contra o StreptInCor e os esplenócitos destes animais, obtidos nessa data, foram utilizados para ensaios de proliferação celular na presença do StreptInCor. Testes de segurança foram efetuados e não observamos reação cruzada contra a miosina cardíaca e após 12 meses de acompanhamento, amostras de tecidos desses animais foram submetidas à análise histológica. Em conclusão não verificamos indícios de reações autoimunes nos animais imunizados com o StreptInCor e os resultados obtidos mostram a capacidade do StreptInCor em desencadear uma resposta imune, duradoura e segura em camundongos portadores de moléculas HLA de classe II
Streptococcal pharyngitis triggered by Streptococcus pyogenes throat infection can result in rheumatic fever (RF) and rheumatic heart disease (RHD) in untreated susceptible individuals. RF is an autoimmune disease that affects more than 20 million children in developing countries. M protein is the major factor of virulence of the bacteria, and it has been studied to develop a vaccine. Currently more than 200 M protein types have been described and its Cterminal domain is conserved in many different serotypes. We developed a vaccine epitope (StreptInCor) composed by 55 amino acid residues of the Cterminal portion of the M protein. In the present work we analyze the ability of the StreptInCor of induce immune response in HLA class II transgenic mice. The transgenic mice harboring the HLA Class II DR2, DR4, DQ6 and DQ8 were immunized subcutaneously with 50 g StreptInCor adsorbed onto 300 g of aluminum hydroxide gel on days 0 and 14. Control groups were immunized with vehicle (Saline) in same conditions. The sera were obtained on day 28 and tested by ELISA to verify the presence of antibodies. The specific cellular immune response was evaluated by proliferation assay using splenocytes. No cross reaction with cardiac myosin were observed. Tissue samples from immunized mice followed by 12 months were analyzed in order to verify if StreptInCor induces some histological damage. No autoimmune or deleterious reactions were observed. In conclusion our results indicate that StreptInCor Induces a good and prolonged and safe immune response in HLA class II transgenic mice
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7

Takejima, Priscila Megumi. "Tipificação do HLA nos fenótipos alérgico e não alérgico da asma." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5146/tde-05102015-111908/.

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A asma é uma doença heterogênea caracterizada por um processo inflamatório crônico das vias aéreas inferiores que está associado ao desenvolvimento da hiperresponsividade brônquica e remodelamento da via aérea. Atualmente, a asma é considerada uma síndrome, ou ao menos uma doença com diversos fenótipos. Tradicionalmente, dois fenótipos são bem definidos pela clínica e exames subsidiários: asma alérgica e asma não alérgica. Eles são diferentes quanto á idade de início, apresentação clínica, história pessoal e familiar de atopia e resposta ao tratamento. Ao contrário da asma alérgica, cuja fisiopatologia está bem caracterizada, a etiologia e mecanismos envolvidos na asma não alérgica não estão bem elucidados. Algumas possibilidades incluem alergia desencadeada por antígenos desconhecidos (fungos), infecção persistente (Chlamydia trachomatis, Mycoplasma sp) e auto-imunidade. Estudos têm descrito em diferentes populações associações entre a asma e alelos/antígenos HLA classe I e II, mas os resultados têm sido inconclusivos. O objetivo deste estudo foi identificar possíveis associações do antígeno leucocitário humano (HLA) classe I (A, B, C) e II (DR, DQ, DP) em pacientes brasileiros com asma alérgica e não alérgica. Um total de 109 pacientes com o diagnóstico de asma (56 com asma alérgica e 53 com asma não alérgica) que estavam em acompanhamento no Serviço de Imunologia Clínica e Alergia do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, e 297 controles (doadores falecidos de órgãos sólidos) tiveram seu sistema HLA classe I (A, B e C) e II (DR, DQ e DP) tipificado. Os pacientes também realizaram espirometria e coletaram sangue para a quantificação da imunoglobulina E (IgE) sérica total e nível sérico de eosinófilos. Além disso, foram avaliados quanto à IgE específica para aeroalergenos através do teste cutâneo de puntura e a pesquisa da IgE sérica específica (ImmunoCAP). O grupo com asma alérgica foi constituído por pacientes que apresentavam resultado positivo para a pesquisa da IgE específica em ambos teste cutâneo de puntura e na investigação in vitro. E o grupo com asma não alérgica apresentava resultados negativos nos dois testes. A comparação do HLA classe I nos grupos estudados identificou frequência significativamente maior do HLA-B*42 e HLA-C*17 no grupo com asma alérgica, enquanto o HLA-B*48 estava estatisticamente associado com o fenótipo não alérgico. Na análise do HLA classe II, o HLA-DPA1*03 e HLA-DPB1*105 apresentou associação com os pacientes com asma alérgica. Concluindo, o estudo observou diferentes associações dos alelos HLA classe I e II com asma alérgica e não alérgica na população brasileira, a qual é caracterizada pela diversidade de origens e miscigenação. Porém, a predisposição genética para asma é poligênica e novos estudos em grandes populações são necessários para confirmar a associação do HLA como fator protetor ou causador da doença
Asthma is a heterogeneous chronic inflammatory disease of lower airways associated with the development of bronchial hyperresponsiveness and airway remodeling. Currently, asthma is regarded as a syndrome or at least a disease with several phenotypes.Traditionally, two phenotypes of asthma have been defined according to clinical and laboratory features: allergic and non-allergic asthma. Each of them has distint age of onset, clinical presentation, personal and family history of allergy and response to therapy. In contrast to allergic asthma, which pathophysiology is well characterized, the etiology and mechanisms involved in non-allergic asthma remain unclear. Some possibilities include allergy triggered by unknow antigens (fungi), persistent infection (Chlamydia trachomatis, Mycoplasma sp) and autoimmunity. Studies have reported associations between asthma and HLA class I and II alleles/antigens in different populations, but the results have been inconclusive. The objective of this study was to identify possible associations of the human leukocyte antigens (HLA) class I (A, B and C) and II (DR, DQ and DP) in Brazilian patients with allergic and non-allergic asthma. A total of 109 patients with asthma (56 with allergic asthma and 53 with non-allergic asthma), who were being followed at the Service of Clinical Immunology and Allergy of the Hospital das Clínicas of the University of São Paulo Medical School, and 297 controls (deceased solid organ donors) had their HLA class I (A,B and C) and II (DR, DQ and DP) typing. Patients performed spirometry and had their blood drawn to measure total serum immunoglobulin E (IgE) levels and eosinophil count. Furthermore, they were assessed for specific IgE to aeroallergens with skin prick test and serum tests (ImmunoCAP). The allergic asthma group was composed of patient presenting positive results for specific IgE in both skin prick test and in vitro assay. And the non-allergic asthma group had negative results in both tests. There were significantly higher frequencies of HLA-B*42 and HLA-C*17 in the allergic asthma group, whereas the HLA-B*48 was associated with the non-allergic group. Regarding HLA class II analysis, HLA-DPA1*03 and HLA DPB1*105 were associated with allergic asthma patients. In conclusion, the study identified different associations of HLA class I and II with allergic and non-allergic asthma in the Brazilian population, which is characterized by diversity of origins and miscegenation. However, the genetic predisposition of asthma is polygenic and new studies on large populations are needed to confirm the role of HLA as a protective or predisposing factor of disease
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Tavares, Marcos Soares. "Estudo caso-controle da região HLA de pacientes com Granulomatose com poliangeíte." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/5/5150/tde-01032017-134802/.

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Os alelos HLA-DPB1*04 e HLA-DRB1*15 estão fortemente associados à Granulomatose com poliangeíte (GPA). Neste estudo, analisamos se os pacientes brasileiros com diagnóstico de GPA apresentam uma base genética na região HLA. Conduzimos um estudo caso-controle, em que analisamos os alelos da região HLA classe I e II em 55 pacientes com diagnóstico de GPA, atendidos no ambulatório de Vasculites Pulmonares do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, e comparamos com os resultados de 110 controles saudáveis. Comparamos também quatro diferentes apresentações clínicas da GPA e a positividade do anticorpo anticitoplasma de neutrófilos (ANCA) com os alelos da região HLA classe I e II. Foi também construída uma árvore de decisões, usando o algoritmo de CART, para a verificação da associação entre os alelos HLA e GPA. Como resultados, observamos que a GPA esteve fortemente associada à presença dos alelos DPB1*04 e DRB1*15 (p = 0,007, odds ratio [OR]: 2,9, 95% intervalo de confiança [IC]: 1,09-3,8; p = 0,006, OR: 2,87, 95% IC: 1,44-4,75, respectivamente) e não à presença do alelo DRB1*04. O alelo DRB1*13 esteve associado com proteção contra GPA (p = 0,042, OR: 0,42, 95% CI: 0,21-0,99). O alelo DPB1*04 esteve significativamente associado a GPA e ANCA-C positivo (OR: 5,47) e à presença de insuficiência renal aguda (p = 0,01037). Concluímos que houve uma interdependência significativa entre os alelos DPB1*0401, DPB1*0402, DRB1*13, C*2 e GPA. Na população estudada, quando o alelo DPB1*04 esteve presente em homozigose, o risco de GPA foi de 81%. Quando o alelo DPB1*0401 esteve ausente ou em heterozigose com o DPB1*0402, como o outro alelo, ou DPB1*0402 esteve em homozigose, o risco da GPA foi de 52,9%. No caso de ausência dos alelos DPB1*0401, DPB1*0402 e DRB1*13, a presença do alelo C*2 aumentou o risco da GPA para 62,5%. Finalmente, na ausência do alelo DPB1*0401 e DPB1*0402 e na presença do alelo DRB1*13, o risco de GPA diminuiu para 0%
The alleles HLA-DPB1*04 and HLA-DRB1*15 are strongly associated with granulomatosis with polyangiitis (GPA). In this study, we examined whether Brazilian patients with GPA had an HLA region genetic background. We conducted a case-control study, in which we analysed alleles of HLA region class I and II from 55 patients with GPA (at the Pulmonary Vasculitis Clinic of the University of São Paulo) and compared the results with those from 110 healthy controls. Comparisons were also performed for 4 different clinical presentations of GPA and anti-neutrophil cytoplasmic antibody (ANCA) positivity and the HLA class I and II region alleles. A tree model decision analysis was conducted using CART algorithm. Our results showed that GPA was strongly associated with alleles DPB1*04 and DRB1*15 (p = 0.007, odds ratio [OR]: 2.9, 95% confidence interval [CI]: 1.09-3.8; p = 0.006, OR: 2.87, 95% CI: 1.44-4.75, respectively) and not with the allele DRB1*04. DRB1*13 allele was associated with protection against GPA (p = 0.042, OR: 0.42, 95% CI: 0.21-0.99). DPB1*04 was significantly associated with GPA plus positive C-ANCA (OR: 5.47) and acute renal failure (p = 0.01037). We concluded that there was a significant interdependence among alleles and GPA. In our population, when allele DPB1*04 was presented in homozygous, the risk of GPA was 81%. When DPB1*0401 allele was absent or heterozygous with DPB1*0402 as the other allele, or DPB1*0402 was homozygous, the risk of disease was 52.9%. If DPB1*0401, DPB1*0402, and DRB1*13 were absent, the presence of C*2 increased the risk of GPA to 62.5%. Finally, in the absence of DPB1*0401 and DPB1*0402 and the presence of DRB1*13, the risk of GPA decreased to 0%
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Painter, Corrie A. "Conformational Lability in MHC II Proteins: A Dissertation." eScholarship@UMMS, 2011. https://escholarship.umassmed.edu/gsbs_diss/539.

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MHC II proteins are heterodimeric glycoproteins that form complexes with antigenic peptides in order to elicit a CD4+ adaptive immune response. Even though there have been numerous MHC II-peptide crystal structures solved, there is little insight into the dynamic process of peptide loading. Through biochemical and biophysical studies, it has been shown that MHC II adopt multiple conformations throughout the peptide loading process. At least one of these conformations is stabilized by the MHC II-like homologue, HLA-DM. The main focus of this thesis is to elucidate alternate conformers of MHC II in an effort to better understand the structural features that enable HLA-DM catalyzed peptide loading. In this thesis, two altered conformations of HLA-DR were investigated, one modeled in the absence of peptide using molecular dynamics, and one stabilized by the mutation αF54C. The model for the peptide-free form of HLA-DR1 was derived from a molecular dynamics simulation. In this model, part of the alpha-subunit extended-strand region proximal to the peptide binding groove is folded into the peptide-binding groove such that the architecture of the critical peptide binding pocket, P1, as well as the invariant hydrogen bonding network were maintained. Biochemical studies aimed at validating the predicted structural changes were consistent with the model generated from the simulations. Next, structural studies were carried out on an MHC II mutant, αF54C, which was shown to have unique peptide binding characteristics as well as enhanced susceptibility to HLA-DM. Although this mutation did not affect the affinity for peptide, there was a striking increase in the rate of intrinsic peptide release. Both αF54C and αF54A were over 100-fold more susceptible to HLADM catalyzed peptide release than wild type as well as other mutants introduced along the peptide binding groove. In addition, mutation of the αF54 position results in a higher affinity for HLA-DM, which, unlike wild type, is detectable by surface plasmon resonance. Crystallographic studies resulted in a 2.3 Å resolution structure for the αF54C-Clip complex. There were two molecules in the asymmetric unit, one of which had no obvious deviations from other MHC II-pep complexes and one which had a conformational change as a result of a crystal contact on the αF51 residue, a residue which has been shown to be involved in the HLA-DM/HLA-DR binding interface. The crystal structure of wild type HLA-DR1- Clip was also solved, but did not have the altered conformation even though there was a similar crystal contact at the αF51. These data suggest the altered conformation seen in the mutant structure, results from increased lability in the extended stand region due to the αF54C mutation. As a result of this work, we have developed a new mechanistic model for how structural features of MHC II influence DM mediated peptide release.
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Hume, Clifford Robert. "Regulation of HLA class II expression in class II negative mutant B-cell lines /." Access full-text from WCMC, 1989. http://proquest.umi.com/pqdweb?did=745028251&sid=1&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Книги з теми "HLA class II geners"

1

Haddad, George E. Expression of HLA class II genes in transgenic mice. Ottawa: National Library of Canada, 1994.

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Michael, Browning, and McMichael Andrew J, eds. HLA and MHC: Genes, molecules and function. Oxford: BIOS Scientific, 1996.

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Solheim, Bjarte G., Erna Møller, and Soldano Ferrone, eds. HLA Class II Antigens. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70367-6.

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1946-, Silver Jack, ed. Molecular biology of HLA class II antigens. Boca Raton, Fla: CRC Press, 1990.

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Natural history of the major histocompatibility complex. New York: Wiley, 1986.

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1940-, Ferrone Soldano, Möller Erna, and Solheim Bjarte G, eds. HLA class II antigens: A comprehensive review of structure and function. Berlin: Springer-Verlag, 1986.

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Glew, Susan Sylvia. HLA Class II antigens and HPV in cervical neoplasia. Manchester: University of Manchester, 1992.

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Rayner, Michelle Louise. The role of polymorphic amino acid residues of HLA class II molecules in susceptibility to type 1A diabetes. Birmingham: University of Birmingham, 2002.

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Savage, David Anthony. Application of DNA techniques to the study of the HLA class II region with reference to renal transplantation and autoimmune disease. [S.l: The Author], 1992.

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Solheim, Bjarte G., Soldano Ferrone, and Erna Moller. HLA Class II Antigens: A Comprehensive Review of Structure and Function. Springer London, Limited, 2012.

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Частини книг з теми "HLA class II geners"

1

Bell, J. I., and H. O. McDevitt. "Molecular Polymorphism of Human Immune-Response-Genes." In HLA Class II Antigens, 442–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70367-6_26.

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Peterson, P. A., and L. Rask. "Genes and Antigens of the HLA-D Region." In HLA Class II Antigens, 1–13. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70367-6_1.

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3

Steinmetz, M. "Structural and Functional Studies of Mouse Class II Genes." In HLA Class II Antigens, 109–27. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70367-6_7.

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Reith, Walter, Sarah Satola, Iris Amaldi, Carlos Herrero Sanchez, Christine Berte, Richard Ulevitch, and Bernard Mach. "Regulation of HLA Class II Genes: Identification of a Regulatory Promoter Binding Protein Missing in Class II-Deficient Congenital Immunodeficiency." In Immunobiology of HLA, 345–47. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-39946-0_130.

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Mach, B., and W. Reith. "Regulation and Deregulation of HLA Class II Genes." In The HLA System in Clinical Transplantation, 82–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77506-2_6.

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Pollack, Marilyn S., Richard G. Cook, Audrey A. Hayes, Samatha Mooney, Neil C. Pedersen, J. David Holcomb, and J. Fielding Hejtmancik. "The Detection of Feline Class I and Class II MHC Homologue Molecules and Genes by Biochemical and Molecular Genetic Techniques." In Immunobiology of HLA, 596–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-39946-0_257.

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Inoko, Hidetoshi, Kimiyoshi Tsuji, Vicky Groves, and John Trowsdale. "Mapping of HLA Class II Genes by Pulsed Field Gel Electrophoresis and Size Polymorphism." In Immunobiology of HLA, 83–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-39946-0_10.

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de Castro, J. A. López. "Class I and Class II HLA Proteins and Genes: An Overview of Structure, Polymorphism, and Expression." In The HLA System in Clinical Transplantation, 49–62. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77506-2_4.

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Nepom, Gerald T., Christine Seyfried, Susan Holbeck, Patricia Byers, Kenneth Wilske, Jerry Palmer, David Robinson, and Barbara Nepom. "HLA-DR4-Associated Disease: Oligonucleotide Probes Identify Specific Class II Susceptibility Genes in Type I Diabetes and Rheumatoid Arthritis." In Immunobiology of HLA, 404–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-39946-0_158.

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Lutke Holzik, M. F., D. J. A. Sonneveld, H. J. Hoekstra, I. M. Nolte, M. Bruinenberg, W. T. A. van der Graaf, D. Th Sleijfer, R. H. Sijmons, C. H. C. M. Buys, and G. J. Te Meerman. "No Association Between HLA Class II Genes and Testicular Germ Tumour (TGCT) with Genotyping of the HLA-Region on Chromosome 6p21 and Haplotype Sharing Analysis." In Germ Cell Tumours V, 45–46. London: Springer London, 2002. http://dx.doi.org/10.1007/978-1-4471-3281-3_8.

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Тези доповідей конференцій з теми "HLA class II geners"

1

Cheng, Hsinyuan, Michael Yi, Michael Bethune, Eric Gschweng, Melinda Au, Duy Nguyen, Kristen Zhang, et al. "210 Generation of hypoimmunogenic allogeneic CAR T cells by inactivation of transcriptional regulators of HLA Class I and II genes." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0210.

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Santos, André Luiz Dos. "EXAMES IMUNOGENÉTICOS PARA AVALIAÇÃO DE COMPATIBILIDADE RECEPTOR-DOADOR EM TRANSPLANTES EM SUMA." In II Congresso Brasileiro de Biologia Molecular On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/2335.

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Introdução: Transplantes são processos onde a compatibilidade Receptor-Doador é fundamental para evitar-se a perda do paciente ou do órgão, que poderia ser melhor transplantado. Para isso, realizam-se múltiplos testes, principalmente clínicos e laboratoriais, avaliando ambos pacientes, buscando sucesso dos transplantes. Objetivo: Reconhecer a importância dos exames imunogenéticos para compatibilidade Receptor-Doador. Material e Métodos: Pesquisa descritiva em documentos científicos em português, no limite de dez anos, no Google Acadêmico e Scielo, destacando os termos: transplantes, imunogenética, rejeição, compatibilidade, combinados entre si, pareando-os. Resultados foram obtidos de um total de sete artigos. Resultados: As avaliações devem considerar a ausência de: (a) contraindicações absolutas - Sorológicas HIV, HTLV I e II, Hepatites B e C; Infecções virais; HIV; Meningoencefalite herpética; Linfoma-leucemia de Células T; Doença por Príons; Neoplasia maligna ativa; Lúpus; Artrite Reumatoide; Esclerodermia e Uso de Drogas. (b) contraindicações relativas - malignidade extra-hepática; SIDA doença e hipertensão pulmonar. (c) contraindicações clinicas - Tumores ativos, infecções não resolvidas (exceto para HIV, HCV, HBV, mas devem ser controlados); rejeição do paciente e expectativa de vida baixa; pacientes desnutridos; pessoas com transtornos mentais ou instabilidade emocional; pessoas que abusam de álcool, tabaco ou outras drogas; (d) contraindicações laboratoriais - Pacientes com doenças e infecções hepáticas e cardiovasculares não controladas. A identidade HLA consiste em vários genes agrupados numa mesma região do cromossomo 6. Sabe-se que mais de 11.000 alelos foram identificados, portanto, é raro que duas pessoas tenham o mesmo conjunto de genes. Porém, mesmo com o uso de imunossupressores para auxiliar o sistema imunológico a se adaptar ao ataque desse corpo estranho, pode ocorrer rejeição do órgão. Os principais exames que inferem contra-indicações são: (a) Tipagem HLA de receptores de transplante de células-tronco hematopoiéticas; (b) Tipagem HLA de doadores de células-tronco hematopoiéticas relevantes; (c) Tipagem HLA de doadores voluntários de células-tronco hematopoiéticas - Fase 1. Busca-se indicadores a presença, no soro do receptor, de anticorpos contra antígenos HLA do doador e identificação de genes HLA classe I e II. Conclusão: Entre as formas de avaliação de contra-indicações para recepção de tecidos, a avaliação laboratorial imunogenética é a mais importante, pois é nela que se saberá a compatibilidade Receptor-Doador.
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Acosta-Colman, I., S. Cabrera-Villalba, G. Avila-Pedretti, M. E. Acosta Hetter, M. Vazquez, A. Ayala Lugo, V. Jolie, et al. "AB0005 Hla class ii in paraguayan immune-mediated inflammatory patients." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.5021.

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"Application of RotaSVM for HLA Class II Protein-Peptide Interaction Prediction." In International Conference on Bioinformatics Models, Methods and Algorithms. SCITEPRESS - Science and and Technology Publications, 2014. http://dx.doi.org/10.5220/0004804801780185.

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Smit, Lidwien A. M., Manolis Kogevinas, Roel Vermeulen, Paul I. W. de Bakker, Emmanuelle Bouzigon, Anne-Elie Carsin, Ivan Curjuric, et al. "HLA Class II Alleles, Occupational Exposures And Asthma: A Candidate Gene-Environment Interaction." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3802.

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Gheerbrant, Hubert, Alicia Guillien, Christian Lupinek, Jean Bousquet, Florence Demenais, Fréderic Gormand, Rachel Nadif, et al. "Associations between allergen-specific IgE sensitization and HLA class II alleles in the EGEA cohort." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.1118.

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Rosha, Deepak, Mohit Chowdhry, Ishan Gupta, and deepak rosha. "Influence of HLA class II DRB1*/DQB1* alleles in phenotypes of Indian patients of sarcoidois." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa703.

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Xue, Jianmin, Bernadette R. Gochuico, Carol A. Feghali-Bostwick, Imre Noth, Steven D. Nathan, Glenn Rosen, Ivan O. Rosas, et al. "The HLA Class II Allele DRB1*1501 Is Over-Represented In Patients With Idiopathic Pulmonary Fibrosis." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4272.

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Paul, Sinu, John Sidney, Bjoern Peters, and Alessandro Sette. "Development and validation of a broad scheme for prediction of HLA class II restricted T cell epitopes." In BCB '14: ACM-BCB '14. New York, NY, USA: ACM, 2014. http://dx.doi.org/10.1145/2649387.2660842.

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Boucher, Tommy, Matthew Davis, Christine Palmer, Tyler Murphy, Andrew Clark, Fujiko Duke, Aaron Yang, et al. "Abstract 4445: MHC class II antigen identification for cancer immunotherapy by deep learning on tumor HLA peptides." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4445.

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Звіти організацій з теми "HLA class II geners"

1

Trucco, Massimo. Children's Hospital of Pittsburgh Histocompatibility Center Microfabricated CE Chips to Make More Cost- Effective HLA Class I and Class II Molecular Typing. Fort Belvoir, VA: Defense Technical Information Center, May 2000. http://dx.doi.org/10.21236/ada377722.

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2

Trucco, Massimo. Children's Hospital of Pittsburgh Histocompatibility Center Nucleotide Sequencing for Detection of Alleles at HLA Class I and Class II Loci on Ethnic Minorities. Fort Belvoir, VA: Defense Technical Information Center, December 1999. http://dx.doi.org/10.21236/ada371509.

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3

Trucco, Massimo. Children's Hospital of Pittsburgh Histocotripatibility Center Molecular Typing of Alleles at HLA Class I and Class II Loci on Blood Spotted Filter Paper. Fort Belvoir, VA: Defense Technical Information Center, January 1999. http://dx.doi.org/10.21236/ada359083.

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