further suggested that treatment with LAG-3-specific humanized agonist Ab, IMP761, can inhibit T cell receptor (TCR)-mediated nuclear factor of activated T-cell (NFAT) activation, and Ag-induced human T cell proliferation and activation, thereby suppressing the symptoms (e.g., cellular infiltration or erythema) of delayed-type hypersensitivity (DTH) in the cynomolgus macaque (27), indicating that LAG-3 signaling is important to suppress autoimmune disorders. This evidence concerns the gene LAG3 and autoimmune disease.