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- W2597122910 abstract "Purpose: In IIM, an increasingly recognised problem is treatment resistant muscle wasting. TNF-? is thought to induce muscle catabolic effects, in part, via nuclear factor kappa B (NF-?B) activation. Several identified genes share homology with the NF-?B family. We investigated the role of NF-?B genes in a large cohort of UK Caucasian IIM patients.Methods: 408 IIM cases (300 adult, 49�14.0 years, 72% female; 108 juvenile, 6�3.6 years 73% female), recruited from the UK Adult Onset Myositis Immunogenetic Collaboration and the Juvenile Dermatomyositis (JDM) National Registry and Repository, were compared to 310 Caucasian controls. Myositis was confirmed as probable/definite (Bohan & Peter, 1975). DNA was genotyped for 56 SNPs in the NF-?B1, NF-?B1A, NF-?B1B, NF-?B1E, I?BL (NF-?BIL1), REL, RELB and BCL3 genes using Sequenom iPlex?. HLA and TNF genotyping were performed as described (Chinoy et al 2006, 2007). Serotyping used radio-immunoprecipitation. Data were stratified by IIM disease subtype (polymyositis [PM], dermatomyositis [DM], myositis/connective tissue disease [CTD]-overlap, JDM) and serotype (anti-synthetase, Mi-2, SRP, U1-RNP, Ku, PM-Scl, 155/140).Results: Significant allele associations were observed in the overall IIM group vs. controls for the IKBL-62T allele (rs2071592), which strengthened after stratification by anti-Jo-1 or -PM-Scl (see table). Genotype analysis revealed an increase of the AT genotype in cases, with a significant association noted under a dominant model (overall IIM group, odds ratio [OR] 2.0, 95% confidence interval [CI] 1.4-2.8, p=1x10-5). No other SNP was significantly associated in the overall IIM group. Strong pairwise linkage disequilibrium (LD) existed between IKBL-62T, TNF-308A and HLA-B*08 (D?=1). Using multivariate logistic regression, the IKBL-62T IIM association was lost after adjusting for either TNF-308A or HLA-B*08.Conclusions: The IKBL-62T allele is associated with IIM, the risk strengthened in anti-Jo-1 and -PM-Scl patients. However, the association is dependent on TNF-308A and HLA-B*08, due to strong shared LD. Thus, after adjustment of the 8.1 haplotype, NF-?B genes do not appear to confer susceptibility in IIM." @default.
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- W2597122910 date "2008-09-01" @default.
- W2597122910 modified "2023-09-23" @default.
- W2597122910 title "Genetic association study of NF-KB genes in UK Caucasian adult and juvenile onset idiopathic inflammatory myopath (IIM)" @default.
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