Abstract

MICA is located at 46 kb centromeric of HLA-B, is highly polymorphic and interactions with NKG2D, its receptor on the surface of NK, Tγδ, and T CD8 lymphocytes. A variation at amino acid position 129 of the α2-heavy chain domain seems to categorize MICA alleles into strong and weak binder of NKG2D receptor, and thereby to influence effector cell function. Our aim was to study allele polymorphism of MICA and the functionally relevant dimorphism (129val/met) of MICA gene in inflammatory bowel disease (IBD) patients in our population. DNA was obtained from IBD patients ( n = 88) and unrelated healthy Murcians ( n = 154) and used to MICA genotyping using polymerase chain reaction-sequence-specific oligonucleotides. We did not find statistical differences in the distribution of MICA alleles between the IBD and control groups. However, we found a higher frequency of MICA-129met/met and a lower frequency of MICA-129val/met genotypes in IBD patients (mainly in ulcerative colitis) than in controls ( pc = 0.02). These preliminary data could suggest a relevant role of MICA-129-val/met SNP (weak/strong binders of NKG2D receptor) in the pathogenesis of IBD.

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