T cell–driven intestinal inflammation is attenuated in the absence of IL-1R signaling. (A) C57BL/6 Rag1^−/− mice were transferred with 4 × 10⁵ CD4⁺ CD25⁻ CD45RB^Hi T cells from C57BL/6 WT mice and culled at the development of clinical signs of disease. cLPLs were isolated from the colon and cultured overnight in complete medium. IL-1β secretion in the supernatants was evaluated by FlowCytoMix kit (eBioscience; mean ± SEM; n = 5 for C57BL/6 Rag1^−/− mice and n = 10 for recipients of CD4⁺CD45Rb^Hi T cells from 2 independent experiments). (B–G) C57BL/6 Rag1^−/− mice were transferred with 4 × 10⁵ CD4⁺ CD25⁻ CD45RB^Hi T cells from C57BL/6 WT or Il1r1^−/− mice. (B) Representative weight loss curve, shown as percentage of initial weight (data are shown as mean ± SEM; n = 8 mice/group, 1 representative of 3 independent experiments). (C and D) Intestinal inflammation scores for the colon (C) and the cecum (D) from three pooled independent experiments. Bars show the mean score. (E) Representative photomicrographs of colon and cecum (bar, 200 µm). (F) Spleen weight and spleen cell number. 1 representative experiment out of 3 is shown (n = 3 for untreated controls and n = 8 for naive CD4⁺ T cell recipients). (G) Cytokine secretion by colonic lamina propria lymphocytes from C57BL/6 Rag1^−/− mice transferred with WT or Il1r1^−/− naive CD4⁺ T cells. Data are shown as mean ± SEM (n = 10–14 from 2 pooled independent experiments). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ND not detectable.