Association of NKG2D gene variants with susceptibility and severity of rheumatoid arthritis

NKG2D
DOI: 10.1111/cei.12891 Publication Date: 2016-10-26T15:32:43Z
ABSTRACT
NKG2D (KLRK1) is a C-type lectin receptor present on natural killer (NK) cells, γδ, CD8+ and CD4+ T cells. Upon ligand binding, mediates activatory co-stimulatory signals to NK cells activated respectively. Polymorphisms in predispose infectious diseases, cancer, transplantation autoimmune disorders. We studied the influence of this polymorphism predisposition modification disease phenotype patients with rheumatoid arthritis (RA). Eight different single nucleotide polymorphisms (SNP) NKG2 gene were genotyped 236 RA 187 controls using Taqman 5' nuclease assays. genotype/allele frequency did not differ between controls. Subgroup analysis showed that A allele NKG2D9 NKG2D10 was significantly higher deformities (a marker severe disease) [11 versus 5%, Pc = 0·03, odds ratio (OR) 2·44, 95% confidence interval (CI) 1·09-5·98 10 4%, 0·04, OR 2·45, CI 1·05-6·39, respectively], while alleles G greater without (Pc 0·41, 0·17-0·91 0·16-0·96). Similar trends association observed deforming female young onset subgroups. Haplotype revealed haplotype G-C-A-G-A-T-C-C than (12 8%, P 1·61, 1·01-2·55), suggesting it may RA. Our study suggests modify risk development severity
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