In line with this finding, our recent studies demonstrated that DR3 deletion in SAMP mice restores the mucosal immunostat, normalizes intestinal inflammatory gene expression, and prevents the development of inflammation-induced intestinal fibrosis, thereby affecting the functions of effector lymphocytes and their capacity to adoptively transfer ileitis (Cominelli et al., unpublished data). The gene discussed is TNFRSF25; the disease is Crohn ileitis.