Over the last decade, we and others showed that tumor necrosis factor receptor 2 (TNFR2) is critical for Treg function and that selective agonism of TNFR2 results in Treg expansion and is therapeutic in inflammatory conditions such as experimental arthritis (46, 47) and graft vs. host disease (48). This evidence concerns the gene TNFRSF1B and arthritic joint disease.