tLTs aggravate DSS-mediated colitis. (A) Histological disease score in RORγt^−/− and wild-type control mice exposed to two cycles of DSS. Scores are shown for eight mice per group from three independent experiments. *, P < 0.01. H&E staining of representative sections from distal colon of RORγt^−/− and wild-type control mice after exposure to two cycles of DSS is shown. Bars, 200 µm. (B) Wasting disease. RORγt^−/− and wild-type control mice were exposed to DSS cycles as indicated, and mouse body weight was assessed at the beginning of every cycle. Shown are weights relative to the starting weight. Data derive from eight mice per group from three independent experiments. *, P < 0.01. (C and D) LTβR blockade ameliorates DSS colitis. Wild-type and RORγt-deficient mice were exposed to two cycles of DSS. RORγt^−/− mice were either treated by weekly i.p. injections of LTβR-Ig protein or with a control Ig. One group of RORγt^−/− mice was treated from birth with a cocktail of antibiotics. Data are shown for six mice per group from two to three independent experiments. *, P < 0.01. Shown is mouse weight at the end of the second DSS cycle in percentage of the starting weight (C) and histological disease score (D). Abx, antibiotic treated. (E) Quantitative real-time PCR on whole colon tissue from untreated wild-type controls and RORγt^−/−, as well as wild-type control mice after exposure to DSS. Ct values were normalized to Gapdh expression. Data shown are for one representative experiment out of three with two mice per group. *, P < 0.05. (F) RORγt^−/− mice were treated with two i.p. injections of 250 µg of neutralizing anti–IFN-γ antibody before the first and the second DSS cycle. Data are shown for one representative experiment out of two with three mice per group. ns, not specific. P > 0.05. Statistical significance was assessed by the paired Student’s t test. Error bars are SD.