| http://purl.uniprot.org/citations/16393997 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/16393997 | http://www.w3.org/2000/01/rdf-schema#comment | "After infection with Mycobacterium tuberculosis, clinical disease usually remains latent, contained by the host immune response. Although polymorphisms of HLA loci have been hypothesized to play a major role in the breakdown of latency, a functional link has not been established. Molecular-based HLA-typing methods were used to test the association of sets of HLA alleles encoding an aspartic acid at codon 57 of the HLA-DQ beta-chain (HLA-DQ beta57-Asp) with susceptibility to tuberculosis in a cohort of 436 pulmonary tuberculosis patients and 107 healthy controls from Cambodia. HLA class II null cells were transduced with HLA-DQ beta57-Asp or HLA-DQ beta57-Ala and evaluated for their ability to bind peptides from two immunogenic M. tuberculosis specific proteins, ESAT-6 and CFP-10. In this study, we report a highly significant association between progressive pulmonary tuberculosis and homozygosity for HLA-DQ beta57-Asp alleles. The presence of HLA-DQ beta57-Asp resulted in a significantly reduced ability to bind a peptide from the central region of the ESAT-6 protein. Furthermore, when this peptide was presented by an HLA-DQ beta57-Asp allele, Ag-specific IFN-gamma production from CD4+ T cells from tuberculosis patients was significantly less than when this peptide was presented by an HLA-DQ-beta allele encoding an alanine at codon 57. Multiple genetic loci and ethnic-specific factors are likely involved in the human immune response to tuberculosis. The data presented here provide a functional explanation for a highly significant association between an HLA polymorphism and tuberculosis in a highly characterized group of patients with susceptibility to progressive tuberculosis infection in Cambodia."xsd:string |
| http://purl.uniprot.org/citations/16393997 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.176.2.1090"xsd:string |
| http://purl.uniprot.org/citations/16393997 | http://purl.uniprot.org/core/author | "Baena A."xsd:string |
| http://purl.uniprot.org/citations/16393997 | http://purl.uniprot.org/core/author | "Delgado J.C."xsd:string |
| http://purl.uniprot.org/citations/16393997 | http://purl.uniprot.org/core/author | "Goldfeld A.E."xsd:string |
| http://purl.uniprot.org/citations/16393997 | http://purl.uniprot.org/core/author | "Thim S."xsd:string |
| http://purl.uniprot.org/citations/16393997 | http://purl.uniprot.org/core/date | "2006"xsd:gYear |
| http://purl.uniprot.org/citations/16393997 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/16393997 | http://purl.uniprot.org/core/pages | "1090-1097"xsd:string |
| http://purl.uniprot.org/citations/16393997 | http://purl.uniprot.org/core/title | "Aspartic acid homozygosity at codon 57 of HLA-DQ beta is associated with susceptibility to pulmonary tuberculosis in Cambodia."xsd:string |
| http://purl.uniprot.org/citations/16393997 | http://purl.uniprot.org/core/volume | "176"xsd:string |
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