DR3- [137] or TL1A-deficient [122] mouse models highlighted the importance of TL1A-DR3 interaction in experimental autoimmune encephalitis (EAE) [138,139], collagen- and antigen-induced arthritis [140] as well as pathological T-cell responses in inflammatory bowel disease [141–144]. Here, TNFRSF25 is linked to inflammatory bowel disease.