Periodontal attachment loss in HIV-infected patients is associated with the major histocompatibility complex 8.1 haplotype (HLA-A1,B8,DR3)
Periodontal attachment loss is mediated by overproduction of tumour necrosis factor (TNF) and interleukin (IL)‐1, and appears to have a genetic component. The 8.1 major histocompatibility complex (MHC) ancestral haplotype (HLA‐A1,B8,TNFA‐308(2),DR3) is associated with elevated TNF production and pre...
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| Published in | Tissue antigens Vol. 54; no. 4; pp. 391 - 399 |
|---|---|
| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Copenhagen
Munksgaard International Publishers
01.10.1999
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0001-2815 1399-0039 |
| DOI | 10.1034/j.1399-0039.1999.540409.x |
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| Abstract | Periodontal attachment loss is mediated by overproduction of tumour necrosis factor (TNF) and interleukin (IL)‐1, and appears to have a genetic component. The 8.1 major histocompatibility complex (MHC) ancestral haplotype (HLA‐A1,B8,TNFA‐308(2),DR3) is associated with elevated TNF production and predisposes carriers to several autoimmune/immunopathological disorders, including rapid progression of HIV disease, but not early onset periodontal disease in healthy individuals. Rather a high proportion of subjects with severe periodontal disease carry allele 2 at IL‐1A−889 and IL‐1B+3953. We predicted that genetic associations may be different or clearer in HIV patients, as they often show elevated production of TNF and IL‐1 and periodontal attachment loss. Hence periodontal parameters and IL‐1 polymorphisms were assessed in HIV‐positive subjects expressing HLA‐B8 with or without other markers of the 8.1 haplotype. Of 16 HLA‐B8 subjects, 13 demonstrated elevated probing pocket depth and clinical attachment loss. The difference was statistically significant and did not correlate with smoking, age, CD4 T‐cell counts, HIV viral load or levels of dental plaque. As TNFA‐308 (allele 2) was present in four non‐B8 subjects who had minimal attachment loss, it may not mediate the effect of the 8.1 haplotype. Moreover, polymorphisms at IL‐1A−889 and IL‐1B+3953 did not significantly affect periodontal parameters. Thus a central MHC gene characteristic of the 8.1 haplotype was the clearest determinant of periodontal attachment loss in HIV‐infected individuals.xm |
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| AbstractList | Periodontal attachment loss is mediated by overproduction of tumour necrosis factor (TNF) and interleukin (IL)‐1, and appears to have a genetic component. The 8.1 major histocompatibility complex (MHC) ancestral haplotype (HLA‐A1,B8,TNFA‐308(2),DR3) is associated with elevated TNF production and predisposes carriers to several autoimmune/immunopathological disorders, including rapid progression of HIV disease, but not early onset periodontal disease in healthy individuals. Rather a high proportion of subjects with severe periodontal disease carry allele 2 at IL‐1A−889 and IL‐1B+3953. We predicted that genetic associations may be different or clearer in HIV patients, as they often show elevated production of TNF and IL‐1 and periodontal attachment loss. Hence periodontal parameters and IL‐1 polymorphisms were assessed in HIV‐positive subjects expressing HLA‐B8 with or without other markers of the 8.1 haplotype. Of 16 HLA‐B8 subjects, 13 demonstrated elevated probing pocket depth and clinical attachment loss. The difference was statistically significant and did not correlate with smoking, age, CD4 T‐cell counts, HIV viral load or levels of dental plaque. As TNFA‐308 (allele 2) was present in four non‐B8 subjects who had minimal attachment loss, it may not mediate the effect of the 8.1 haplotype. Moreover, polymorphisms at IL‐1A−889 and IL‐1B+3953 did not significantly affect periodontal parameters. Thus a central MHC gene characteristic of the 8.1 haplotype was the clearest determinant of periodontal attachment loss in HIV‐infected individuals.xm Periodontal attachment loss is mediated by overproduction of tumour necrosis factor (TNF) and interleukin (IL)-1, and appears to have a genetic component. The 8.1 major histocompatibility complex (MHC) ancestral haplotype (HLA-A1,B8,TNFA-308(2),DR3) is associated with elevated TNF production and predisposes carriers to several autoimmune/immunopathological disorders, including rapid progression of HIV disease, but not early onset periodontal disease in healthy individuals. Rather a high proportion of subjects with severe periodontal disease carry allele 2 at IL-1A-889 and IL-1B+3953. We predicted that genetic associations may be different or clearer in HIV patients, as they often show elevated production of TNF and IL-1 and periodontal attachment loss. Hence periodontal parameters and IL-1 polymorphisms were assessed in HIV-positive subjects expressing HLA-B8 with or without other markers of the 8.1 haplotype. Of 16 HLA-B8 subjects, 13 demonstrated elevated probing pocket depth and clinical attachment loss. The difference was statistically significant and did not correlate with smoking, age, CD4 T-cell counts, HIV viral load or levels of dental plaque. As TNFA-308 (allele 2) was present in four non-B8 subjects who had minimal attachment loss, it may not mediate the effect of the 8.1 haplotype. Moreover, polymorphisms at IL-1A-889 and IL-1B+3953 did not significantly affect periodontal parameters. Thus a central MHC gene characteristic of the 8.1 haplotype was the clearest determinant of periodontal attachment loss in HIV-infected individuals.Periodontal attachment loss is mediated by overproduction of tumour necrosis factor (TNF) and interleukin (IL)-1, and appears to have a genetic component. The 8.1 major histocompatibility complex (MHC) ancestral haplotype (HLA-A1,B8,TNFA-308(2),DR3) is associated with elevated TNF production and predisposes carriers to several autoimmune/immunopathological disorders, including rapid progression of HIV disease, but not early onset periodontal disease in healthy individuals. Rather a high proportion of subjects with severe periodontal disease carry allele 2 at IL-1A-889 and IL-1B+3953. We predicted that genetic associations may be different or clearer in HIV patients, as they often show elevated production of TNF and IL-1 and periodontal attachment loss. Hence periodontal parameters and IL-1 polymorphisms were assessed in HIV-positive subjects expressing HLA-B8 with or without other markers of the 8.1 haplotype. Of 16 HLA-B8 subjects, 13 demonstrated elevated probing pocket depth and clinical attachment loss. The difference was statistically significant and did not correlate with smoking, age, CD4 T-cell counts, HIV viral load or levels of dental plaque. As TNFA-308 (allele 2) was present in four non-B8 subjects who had minimal attachment loss, it may not mediate the effect of the 8.1 haplotype. Moreover, polymorphisms at IL-1A-889 and IL-1B+3953 did not significantly affect periodontal parameters. Thus a central MHC gene characteristic of the 8.1 haplotype was the clearest determinant of periodontal attachment loss in HIV-infected individuals. Periodontal attachment loss is mediated by overproduction of tumour necrosis factor (TNF) and interleukin (IL)-1, and appears to have a genetic component. The 8.1 major histocompatibility complex (MHC) ancestral haplotype (HLA-A1,B8,TNFA-308(2),DR3) is associated with elevated TNF production and predisposes carriers to several autoimmune/immunopathological disorders, including rapid progression of HIV disease, but not early onset periodontal disease in healthy individuals. Rather a high proportion of subjects with severe periodontal disease carry allele 2 at IL-1A-889 and IL-1B+3953. We predicted that genetic associations may be different or clearer in HIV patients, as they often show elevated production of TNF and IL-1 and periodontal attachment loss. Hence periodontal parameters and IL-1 polymorphisms were assessed in HIV-positive subjects expressing HLA-B8 with or without other markers of the 8.1 haplotype. Of 16 HLA-B8 subjects, 13 demonstrated elevated probing pocket depth and clinical attachment loss. The difference was statistically significant and did not correlate with smoking, age, CD4 T-cell counts, HIV viral load or levels of dental plaque. As TNFA-308 (allele 2) was present in four non-B8 subjects who had minimal attachment loss, it may not mediate the effect of the 8.1 haplotype. Moreover, polymorphisms at IL-1A-889 and IL-1B+3953 did not significantly affect periodontal parameters. Thus a central MHC gene characteristic of the 8.1 haplotype was the clearest determinant of periodontal attachment loss in HIV-infected individuals. |
| Author | Price, P. Calder, D.M. Rogers, M. Witt, C.S. Allcock, R.J.N. French, M.A. Davies, G.R. Christiansen, F.T. Baluchova, K. Moore, C.B. Cameron, P.U. |
| Author_xml | – sequence: 1 givenname: P. surname: Price fullname: Price, P. organization: Department of Clinical Immunology, Royal Perth Hospital, Perth, and Department of Pathology, University of Western Australia, Nedlands, Western Australia – sequence: 2 givenname: D.M. surname: Calder fullname: Calder, D.M. organization: School of Oral Health Sciences, University of Western Australia, Nedlands, Western Australia – sequence: 3 givenname: C.S. surname: Witt fullname: Witt, C.S. organization: Department of Clinical Immunology, Royal Perth Hospital, Perth, and Department of Pathology, University of Western Australia, Nedlands, Western Australia – sequence: 4 givenname: R.J.N. surname: Allcock fullname: Allcock, R.J.N. organization: Department of Clinical Immunology, Royal Perth Hospital, Perth, and Department of Pathology, University of Western Australia, Nedlands, Western Australia – sequence: 5 givenname: F.T. surname: Christiansen fullname: Christiansen, F.T. – sequence: 6 givenname: G.R. surname: Davies fullname: Davies, G.R. organization: School of Oral Health Sciences, University of Western Australia, Nedlands, Western Australia – sequence: 7 givenname: P.U. surname: Cameron fullname: Cameron, P.U. organization: Department of Microbiology and Immunology, University of Melbourne, Victoria, Australia – sequence: 8 givenname: M. surname: Rogers fullname: Rogers, M. organization: Department of Clinical Immunology, Royal Perth Hospital, Perth, and Department of Pathology, University of Western Australia, Nedlands, Western Australia – sequence: 9 givenname: K. surname: Baluchova fullname: Baluchova, K. – sequence: 10 givenname: C.B. surname: Moore fullname: Moore, C.B. organization: Mathematics and Statistics, Murdoch University, Murdoch, Western Australia – sequence: 11 givenname: M.A. surname: French fullname: French, M.A. organization: Department of Clinical Immunology, Royal Perth Hospital, Perth, and Department of Pathology, University of Western Australia, Nedlands, Western Australia |
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| Snippet | Periodontal attachment loss is mediated by overproduction of tumour necrosis factor (TNF) and interleukin (IL)‐1, and appears to have a genetic component. The... Periodontal attachment loss is mediated by overproduction of tumour necrosis factor (TNF) and interleukin (IL)-1, and appears to have a genetic component. The... |
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| SubjectTerms | Adult Alleles Haplotypes histocompatibility antigen HLA HIV HIV Infections - complications HIV Infections - genetics HIV Infections - immunology HLA Antigens - genetics HLA Antigens - immunology HLA-A1 Antigen - genetics HLA-A1 Antigen - immunology HLA-B8 Antigen - genetics HLA-B8 Antigen - immunology HLA-DR3 Antigen - genetics HLA-DR3 Antigen - immunology Human immunodeficiency virus Humans interleukin-1 Interleukin-1 - genetics Male MHC Periodontal Attachment Loss - genetics Periodontal Attachment Loss - immunology Periodontal Attachment Loss - virology periodontal disease Phenotype Polymorphism, Genetic Severity of Illness Index TNF Tumor Necrosis Factor-alpha - genetics |
| Title | Periodontal attachment loss in HIV-infected patients is associated with the major histocompatibility complex 8.1 haplotype (HLA-A1,B8,DR3) |
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