Cargando…

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...

Descripción completa

Detalles Bibliográficos
Autores principales: Fechtenbaum, Marie, Desoutter, Judith, Delvallez, Gauthier, Brochot, Etienne, Guillaume, Nicolas, Goëb, Vincent
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
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
_version_ 1783455075799138304
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
work_keys_str_mv AT fechtenbaummarie micaandnkg2dvariantsasriskfactorsinspondyloarthritisacasecontrolstudy
AT desoutterjudith micaandnkg2dvariantsasriskfactorsinspondyloarthritisacasecontrolstudy
AT delvallezgauthier micaandnkg2dvariantsasriskfactorsinspondyloarthritisacasecontrolstudy
AT brochotetienne micaandnkg2dvariantsasriskfactorsinspondyloarthritisacasecontrolstudy
AT guillaumenicolas micaandnkg2dvariantsasriskfactorsinspondyloarthritisacasecontrolstudy
AT goebvincent micaandnkg2dvariantsasriskfactorsinspondyloarthritisacasecontrolstudy