Furthermore, similar to the recent report that KIR+CD8+ T cells are regulatory via their capacity to suppress pathogenic T cells and are active in autoimmune diseases and COVID-19 (33), we found that the nasal Foralumab treated CD8+ TEMRA show induction of KIR3DL2 in addition to TIGIT, KLRG1 and TGFB1, while LAP (TGFb), TIGIT and KLRG1 are induced on in vitro Foralumab-stimulated CD8 T cells. This evidence concerns the gene KIR3DL2 and autoimmune disease.