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MICA and NKG2D variants as risk factors in spondyloarthritis: a case–control study
The major histocompatibility complex class I polypeptide-related sequence A (MICA) glycoprotein mediates the activation of the natural killer group 2D receptor (NKG2D) expressed on NK and CD8+ T cells. A methionine or valine at position 129 in exon 3 results in strong (MICA129 met) or weak (MICA129...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6768283/ https://www.ncbi.nlm.nih.gov/pubmed/30177859 http://dx.doi.org/10.1038/s41435-018-0044-x |
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author | Fechtenbaum, Marie Desoutter, Judith Delvallez, Gauthier Brochot, Etienne Guillaume, Nicolas Goëb, Vincent |
author_facet | Fechtenbaum, Marie Desoutter, Judith Delvallez, Gauthier Brochot, Etienne Guillaume, Nicolas Goëb, Vincent |
author_sort | Fechtenbaum, Marie |
collection | PubMed |
description | The major histocompatibility complex class I polypeptide-related sequence A (MICA) glycoprotein mediates the activation of the natural killer group 2D receptor (NKG2D) expressed on NK and CD8+ T cells. A methionine or valine at position 129 in exon 3 results in strong (MICA129 met) or weak (MICA129 val) binding to NKG2D. The MICA A5.1 allele causes a premature stop codon. Various NKG2D polymorphisms are associated with low (NKC3 C/C and NKC4 C/C) or high (NKC3 G/G and NKC4 T/T) levels of NK cell cytotoxic activity. In 162 patients with spondyloarthritis (115 with ankylosing spondyloarthritis, 46 with psoriatic arthritis and 1 with reactive arthritis) compared to 124 healthy controls, MICA-129 with methionine allele was more frequent in patients with spondyloarthritis (odds ratio (OR) (95% confidence interval) = 4.84 (2.75‒8.67)), whereas MICA-129 val/val, MICA A5.1 and NKC3 C/C variants were less frequent (OR = 0.20 (0.11‒0.37), 0.15 (0.06‒0.36) and 0.24 (0.13‒0.44), respectively). After adjustment for HLA-B*27 status, only NKC3 C/C remained linked to spondyloarthritis (adjusted OR = 0.14 (0.06‒0.33)). Homozygosity for MICA A5.1 is linked to ankylosing spondyloarthritis, and NKC3 C/C and MICA-129 val/val to psoriatic arthritis. MICA and NKC3 polymorphisms (related to a low NK cell cytotoxic activity) constituted a genetic association with spondyloarthritis. |
format | Online Article Text |
id | pubmed-6768283 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-67682832019-10-02 MICA and NKG2D variants as risk factors in spondyloarthritis: a case–control study Fechtenbaum, Marie Desoutter, Judith Delvallez, Gauthier Brochot, Etienne Guillaume, Nicolas Goëb, Vincent Genes Immun Article The major histocompatibility complex class I polypeptide-related sequence A (MICA) glycoprotein mediates the activation of the natural killer group 2D receptor (NKG2D) expressed on NK and CD8+ T cells. A methionine or valine at position 129 in exon 3 results in strong (MICA129 met) or weak (MICA129 val) binding to NKG2D. The MICA A5.1 allele causes a premature stop codon. Various NKG2D polymorphisms are associated with low (NKC3 C/C and NKC4 C/C) or high (NKC3 G/G and NKC4 T/T) levels of NK cell cytotoxic activity. In 162 patients with spondyloarthritis (115 with ankylosing spondyloarthritis, 46 with psoriatic arthritis and 1 with reactive arthritis) compared to 124 healthy controls, MICA-129 with methionine allele was more frequent in patients with spondyloarthritis (odds ratio (OR) (95% confidence interval) = 4.84 (2.75‒8.67)), whereas MICA-129 val/val, MICA A5.1 and NKC3 C/C variants were less frequent (OR = 0.20 (0.11‒0.37), 0.15 (0.06‒0.36) and 0.24 (0.13‒0.44), respectively). After adjustment for HLA-B*27 status, only NKC3 C/C remained linked to spondyloarthritis (adjusted OR = 0.14 (0.06‒0.33)). Homozygosity for MICA A5.1 is linked to ankylosing spondyloarthritis, and NKC3 C/C and MICA-129 val/val to psoriatic arthritis. MICA and NKC3 polymorphisms (related to a low NK cell cytotoxic activity) constituted a genetic association with spondyloarthritis. Nature Publishing Group UK 2018-09-04 2019 /pmc/articles/PMC6768283/ /pubmed/30177859 http://dx.doi.org/10.1038/s41435-018-0044-x Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Fechtenbaum, Marie Desoutter, Judith Delvallez, Gauthier Brochot, Etienne Guillaume, Nicolas Goëb, Vincent MICA and NKG2D variants as risk factors in spondyloarthritis: a case–control study |
title | MICA and NKG2D variants as risk factors in spondyloarthritis: a case–control study |
title_full | MICA and NKG2D variants as risk factors in spondyloarthritis: a case–control study |
title_fullStr | MICA and NKG2D variants as risk factors in spondyloarthritis: a case–control study |
title_full_unstemmed | MICA and NKG2D variants as risk factors in spondyloarthritis: a case–control study |
title_short | MICA and NKG2D variants as risk factors in spondyloarthritis: a case–control study |
title_sort | mica and nkg2d variants as risk factors in spondyloarthritis: a case–control study |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6768283/ https://www.ncbi.nlm.nih.gov/pubmed/30177859 http://dx.doi.org/10.1038/s41435-018-0044-x |
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