Correction: Pharmacological Inhibition of MEK-ERK Signaling Enhances Th17 Differentiation

ERK-inhibited Th17 cells precipitated early onset and more severe colitis. Th cells were cultured as in Fig. 2A. PBS or 5 × 10⁵ in vitro differentiated cells were transferred i.p. into Rag^–/– mice (PBS group, n = 5; no cytokine group, n = 5; no cytokine + U0126 group, n = 5; TGF-β + IL-6 group, n = 8; TGF-β + IL-6 + U0126, n = 7). The progression of wasting disease was monitored in terms of (A) change of body weights of mice expressed as a percent of their original weights and (B) degree of intestinal damage and leukocyte infiltration as assessed by histologic analysis of the distal colons of mice sacrificed 35–45 d (i) or 70–80 d (ii) after transfer. Features shown are representative sections from one mouse of three mice per treatment group (original magnification ×4). C, Th cells were isolated from mesenteric lymph nodes of mice that initially received untreated Th17 (TGF-β + IL-6) or ERK-inhibited Th17 (TGF-β + IL-6 + U0126) cells during phase i or ii. The cells were then seeded at 2 × 10⁶/ml, stimulated with PMA and ionomycin in the presence of GolgiPlug Inhibitor for 6 h and assessed for their ex vivo expression of IL-17A and IFN-γ. D, Real-time RT-PCR to quantify the levels of il-22 transcript in Th cells isolated as in C. Data shown are representative of two independent experiments.