In coeliac disease, where there is chronic heightened expression of IL-15 by stressed epithelial cells, increased expression of CD94 and the activating CD94/NKG2C heterodimer, with a concomitant decrease of NKG2A on T-IEL has been observed.104,108 CD8+ TCRγδ T-IEL that express NKG2A are also decreased in active coeliac disease and these cells can suppress the cytotoxic programming of TCRαβ T-IEL, dependent on CD94/NKG2A engagement and TGFβ production.109 This suggests CD94 inhibitory function is lost in coeliac disease. This evidence concerns the gene KLRD1 and celiac disease.