In this context, human RA synovium and synovial fluid have been reported to be “enriched” with PD-1-expressing T cells, while in a murine model of experimental arthritis, PD-1 gene knockout mice (PD-1−/−) demonstrated increased susceptibility for development of collagen-induced arthritis, which was associated with increased T cell proliferation and production of IFN-γ and IL-17 (89). This evidence concerns the gene IFNG and rheumatoid arthritis.