BTN2A2 appears to dampen dysregulated T cell activity associated with autoimmunity, as the exogenous administration of BTN2A2-IgG2a Fc proteins ameliorated the pathogenicity of a disease modeling rheumatoid arthritis in mice through the impairment of T cell proliferation and production of Th1/Th17 cytokines [42]. This evidence concerns the gene BTN2A2 and rheumatoid arthritis.