Notably, in lupus, NKG2D+ CD4+ T cells appear to be immunosuppressive [132], but in GCA, NKG2D has been reported to enhance the pathogenicity of Th1 and Th17 cells and stimulate the release of pro-inflammatory cytokines such as IFNγ and Granulocyte–macrophage colony-stimulating factor (GM-CSF), which are both important pathogenic players [129, 133, 134]. The gene discussed is KLRK1; the disease is temporal arteritis.