Tan, A. H.-M., and K.-P. Lam. 2010. Pharmacological inhibition of MEK–ERK signaling enhances Th17 differentiation. J. Immunol. 184: 1849–1857.

In Fig. 6B of our article, the wrong histological image corresponding to phase i of the “no cytokine group” was shown. The authors wish to replace the panel with the correct image. This replacement figure represents data obtained from the same experiment, and performed at the same time, as the rest of the data in the figure. The figure legend and main conclusions of the article remain unchanged.

FIGURE 6.

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.

FIGURE 6.

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.

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The corrected figure is below. The figure legend was correct as published and is shown below for reference. We regret any confusion and inconvenience this may have caused.