rs1051792, also known as MICA-129, Val129Met and V129M, is a G>A transition at residue 129 of the MHC class I polypeptide-related sequence A MICA gene.
It has been found in the same training cohort as above that the A allele in the patient and the donor (p=0.066 and 0.013) is associated with a reduced overall survival and an increased risk of relapse (p=0.007 and p=0.003). According to these results, the presence of the G allele in the patient associated with the incidence of cGvHD (p=0.002) and patients homozygous to the A allele had an increased risk of relapse (p=0.02). In contrast to HLA-E molecules, which are ligands for inhibitory NK receptors, MICA is ligand for activating NKG2D receptors. Patient who are homozygous for a valine at residue 129 of MICA are at higher risk of chronic GvHD after HLA-matched sibling HCT in comparison to patient who have a methionine at this position. This risk was independent of acute GvHD, suggesting that the residue 129 play a role in alloimmune responses and thus maybe protective against GvHD, (Boukouaci W, et al. 2009). MICA mismatching between patient and donor has a great influence on the clinical outcome because of the fact that MICA is polymorphic with over 84 recognized unique alleles (http://hla.alleles.org). According to two studies done to evaluate the role of mismatching MICA genes and risk of acute GvHD, it was shown that MICA mismatching was associated with an increased risk of grades II-IV acute GvHD but not grades III-IV acute GvHD in both HLA matched and mismatched transplant, and that was correlated notably with the GvHD of the GI tract (P=0.05). (Parmar S, et al. 2009), (Anderson E, et al. 2009).
[PMID 19409079] Association of MICA with rheumatoid arthritis independent of known HLA-DRB1 risk alleles in a family-based and a case control study
[PMID 21702010] Role of the MICA polymorphism in systemic lupus erythematosus.