Abstract
MHC class I polypeptide-related sequence A (MICA) is a stress-induced protein involved in activation of NK and T cells through interaction with NKG2D receptor. These molecules are atypically expressed in synovium of patients diagnosed with rheumatoid arthritis (RA). A total of 279 patients with RA, qualified to TNF-blockade therapy, were genotyped for MICA rs1051792 SNP. The effectiveness of anti-TNF agents was assessed with European League Against Rheumatism criteria. Significant relationship between MICA rs1051792 and outcome of TNF-blockade therapy has been found. The MICA rs1051792 GG genotype was overrepresented in patients non-responsive to anti-TNF drugs in comparison with other genotypes (p = 0.010). On the other hand, beneficial therapeutic response was more frequently detected among RA subjects possessing heterozygous genotype than those with homozygous genotypes (p = 0.003). Furthermore, increased MICA concentrations in serum were observed in patients possessing MICA rs1051792 GG genotype as compared with those with GA or AA genotypes (p = 1.8 × 10−5). The results from this study indicate the potential influence of MICA rs1051792 polymorphism on modulation of therapeutic response to TNF-blockade treatment in RA.
Highlights
Rheumatoid arthritis (RA) is a chronic inflammatory disorder with a worldwide prevalence of around 1% and predominance in females [1, 2]
Since MHC class I polypeptide-related sequence A (MICA) is expressed under pathological conditions, it constitutes a significant part of host defence system, resulting in detection and eradication of abnormal cells
Dysregulation of the signalling pathway mediated by MICA molecules may trigger self-aggression and promote proinflammatory process underlying the development of autoimmune diseases
Summary
Rheumatoid arthritis (RA) is a chronic inflammatory disorder with a worldwide prevalence of around 1% and predominance in females [1, 2]. TNF-blockade therapy constitutes a spectacular advance in the RA treatment, approximately one-third of patients do not respond to this therapeutic approach [9, 10]. Biologic mechanisms underlying this nonresponsiveness to anti-TNF treatment remain obscure, inefficiency of therapy might be partially determined by genetic heterogeneity among patients.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
