{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,20]],"date-time":"2026-01-20T11:48:23Z","timestamp":1768909703721,"version":"3.49.0"},"reference-count":38,"publisher":"Springer Science and Business Media LLC","issue":"3","license":[{"start":{"date-parts":[[2009,5,1]],"date-time":"2009-05-01T00:00:00Z","timestamp":1241136000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/2.0\/"},{"start":{"date-parts":[[2009,5,1]],"date-time":"2009-05-01T00:00:00Z","timestamp":1241136000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/2.0\/"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Arthritis Res Ther"],"abstract":"<jats:title>Abstract<\/jats:title><jats:sec>\n                        <jats:title>Introduction<\/jats:title>\n                        <jats:p>The gene <jats:italic>MICA<\/jats:italic> encodes the protein major histocompatibility complex class I polypeptide-related sequence A. It is expressed in synovium of patients with rheumatoid arthritis (RA) and its implication in autoimmunity is discussed. We analyzed the association of genetic variants of <jats:italic>MICA<\/jats:italic> with susceptibility to RA.<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Methods<\/jats:title>\n                        <jats:p>Initially, 300 French Caucasian individuals belonging to 100 RA trio families were studied. An additional 100 independent RA trio families and a German Caucasian case-control cohort (90\/182 individuals) were available for replication. As <jats:italic>MICA<\/jats:italic> is situated in proximity to known risk alleles of the <jats:italic>HLA-DRB1<\/jats:italic> locus, our analysis accounted for linkage disequilibrium either by analyzing the subgroup consisting of parents not carrying <jats:italic>HLA-DRB1<\/jats:italic> risk alleles with transmission disequilibrium test (TDT) or by implementing a regression model including all available data. Analysis included a microsatellite polymorphism (GCT)n and single-nucleotide polymorphisms (SNPs) rs3763288 and rs1051794.<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Results<\/jats:title>\n                        <jats:p>In contrast to the other investigated polymorphisms, the non-synonymously coding SNP <jats:italic>MICA<\/jats:italic>-250 (rs1051794, Lys196Glu) was strongly associated in the first family cohort (TDT: <jats:italic>P<\/jats:italic> = 0.014; regression model: odds ratio [OR] 0.46, 95% confidence interval [CI] 0.25 to 0.82, <jats:italic>P<\/jats:italic> = 0.007). Although the replication family sample showed only a trend, combined family data remained consistent with the hypothesis of <jats:italic>MICA<\/jats:italic>-250 association independent from shared epitope (SE) alleles (TDT: <jats:italic>P<\/jats:italic> = 0.027; regression model: OR 0.56, 95% CI 0.38 to 0.83, <jats:italic>P<\/jats:italic> = 0.003). We also replicated the protective association of <jats:italic>MICA<\/jats:italic>-250A within a German Caucasian cohort (OR 0.31, 95% CI 0.1 to 0.7, <jats:italic>P<\/jats:italic> = 0.005; regression model: OR 0.6, 95% CI 0.37 to 0.96, <jats:italic>P<\/jats:italic> = 0.032). We showed complete linkage disequilibrium of <jats:italic>MICA<\/jats:italic>-250 (D' = 1, <jats:italic>r<\/jats:italic><jats:sup>\n                              <jats:italic>2<\/jats:italic>\n                           <\/jats:sup>= 1) with the functional <jats:italic>MICA<\/jats:italic> variant rs1051792 (D' = 1, <jats:italic>r<\/jats:italic><jats:sup>\n                              <jats:italic>2<\/jats:italic>\n                           <\/jats:sup>= 1). As rs1051792 confers differential allelic affinity of MICA to the receptor NKG2D, this provides a possible functional explanation for the observed association.<\/jats:p>\n                     <\/jats:sec><jats:sec>\n                        <jats:title>Conclusions<\/jats:title>\n                        <jats:p>We present evidence for linkage and association of <jats:italic>MICA<\/jats:italic>-250 (rs1051794) with RA independent of known <jats:italic>HLA-DRB1<\/jats:italic> risk alleles, suggesting <jats:italic>MICA<\/jats:italic> as an RA susceptibility gene. However, more studies within other populations are necessary to prove the general relevance of this polymorphism for RA.<\/jats:p>\n                     <\/jats:sec>","DOI":"10.1186\/ar2683","type":"journal-article","created":{"date-parts":[[2009,5,20]],"date-time":"2009-05-20T19:30:54Z","timestamp":1242847854000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":42,"title":["Association of MICA with rheumatoid arthritis independent of known HLA-DRB1risk alleles in a family-based and a case control study"],"prefix":"10.1186","volume":"11","author":[{"given":"Holger","family":"Kirsten","sequence":"first","affiliation":[]},{"given":"Elisabeth","family":"Petit-Teixeira","sequence":"additional","affiliation":[]},{"given":"Markus","family":"Scholz","sequence":"additional","affiliation":[]},{"given":"Dirk","family":"Hasenclever","sequence":"additional","affiliation":[]},{"given":"Helene","family":"Hantmann","sequence":"additional","affiliation":[]},{"given":"Dirk","family":"Heider","sequence":"additional","affiliation":[]},{"given":"Ulf","family":"Wagner","sequence":"additional","affiliation":[]},{"given":"Ulrich","family":"Sack","sequence":"additional","affiliation":[]},{"given":"Vitor","family":"Hugo Teixeira","sequence":"additional","affiliation":[]},{"given":"Bernard","family":"Prum","sequence":"additional","affiliation":[]},{"given":"Jana","family":"Burkhardt","sequence":"additional","affiliation":[]},{"given":"C\u00e9line","family":"Pierlot","sequence":"additional","affiliation":[]},{"given":"Frank","family":"Emmrich","sequence":"additional","affiliation":[]},{"given":"Fran\u00e7ois","family":"Cornelis","sequence":"additional","affiliation":[]},{"given":"Peter","family":"Ahnert","sequence":"additional","affiliation":[]}],"member":"297","published-online":{"date-parts":[[2009,5,1]]},"reference":[{"key":"2523_CR1","doi-asserted-by":"publisher","first-page":"853","DOI":"10.1002\/art.20693","volume":"51","author":"C Turesson","year":"2004","unstructured":"Turesson C, Weyand CM, Matteson EL: Genetics of rheumatoid arthritis: is there a pattern predicting extraarticular manifestations?. 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