The transcription factor IFN regulatory factor–4 controls experimental colitis in mice via T cell–derived IL-6
J. Clin. Invest. Jonas Mudter, et al. 118:2415 doi:10.1172/JCI33227 [Go to this article.]

Figure 8
The protective effects of IRF4 deficiency are mediated via T lymphocytes: studies in the CD45RB^hi adoptive transfer model of colitis. CD45RB^hiCD4⁺ T cells from WT or IRF4^–/– mice were adoptively transferred into immunodeficient RAG2^–/– mice. Whereas RAG2^–/– mice reconstituted with WT T cells developed severe colitis accompanied by weight loss (A, red curve), mice given IRF4^–/– T cells were completely protected and even gained body weight (A, blue curve). One representative experiment out of 3 with 4 to 7 mice per group is shown. The differences between both groups were significant at days 14 and 15. (B) Endoscopy showed an inflamed mucosa in RAG2-knockout mice given WT T cells, whereas little or no inflammation was noted in RAG2^–/– mice reconstituted with IRF4-deficient T cells. (C) Consistently, histological scoring (n = 8 per group) revealed significantly reduced colitis activity in the latter as compared with the former group of mice (**P < 0.01). Whereas the WT group showed marked inflammation, only a very mild colitis was noted in the IRF4-deficient group. (D) For each group, representative endoscopic and histologic pictures are shown. Original magnification, ×100.