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 6
The protective effect of IRF4 deficiency is abrogated in TNBS and oxazolone colitis by administration of recombinant IL-6 or hyper–IL-6. (A) To determine the functional role of IL-6 signaling for the effects of IRF4 on TNBS colitis activity in vivo, recombinant IL-6 or the designer fusion protein hyper–IL-6 was intraperitoneally administered to TNBS-treated IRF4-deficient mice. TNBS-treated IRF4^–/– mice exhibited severe inflammation and weight loss upon IL-6 or hyper–IL-6 treatment that was indistinguishable from colitis in WT control mice (TNBS-treated IRF4^–/– plus hyper–IL-6 versus TNBS-treated IRF4^–/– without hyper–IL-6; *P < 0.05). Data are given as mean values ± SEM (IRF4^+/+ plus TNBS, n = 6; IRF4^–/– plus TNBS, n = 7; IRF4^–/– plus TNBS and hyper–IL-6, n = 5; IRF4^–/– plus TNBS and hyper–IL-6, n = 5; IRF4^+/+ plus TNBS and IL-6, n = 4; IRF4^–/– plus TNBS and hyper–IL-6, n = 5, in 2 independent experiments). (B) To determine the functional role of IL-6 signaling for the effects of IRF4 on oxazolone colitis activity in vivo, hyper–IL-6 was intraperitoneally administered to oxazolone-treated IRF4-deficient mice. Oxazolone-treated IRF4^–/– mice exhibited severe inflammation and weight loss upon hyper–IL-6 treatment that was indistinguishable from colitis in WT control mice (oxazolone-treated IRF4^–/– plus hIL6 versus oxazolone-treated IRF4^–/– without hIL6). Data are given as mean values ± SEM (IRF4^+/+ plus oxazolone [oxa], n = 12; IRF4^–/– plus oxazolone, n = 13; IRF4^–/– plus oxazolone plus hyper–IL-6, n = 7; IRF4^+/+ plus oxazolone plus hyper–IL-6, n = 6, in 3 independent experiments).