Sun, M., C. He, L. Chen, W. Yang, W. Wu, F. Chen, A. T. Cao, S. Yao, S. M. Dann, T. G. M. Dhar, L. Salter-Cid, Q. Zhao, Z. Liu, and Y. Cong. 2019. RORγt represses IL-10 production in Th17 cells to maintain their pathogenicity in inducing intestinal inflammation. J. Immunol. 202: 79–92.
In the original version of this article, the top image depicting Rag–/– recipients of Th17 cells in (Fig. 5A was incorrect. The corrected version of (Fig. 5 is shown below. The figure has been corrected in the online of the article, which now differs from the print version as originally published. The figure legend was correct as published and is shown below for reference.
Treatment with anti–IL-10R mAb increases severity of colitis induced by RORγt inhibitor–treated Th17 cells. Splenic CD4+ T cells from CBir1 Tg mice were cultured under Th17-polarization conditions ± RORγt inhibitor (1 μM) for 5 d, and 1 × 106 T cells were i.v. injected into groups of Rag−/− mice (n = 5–6 per group), respectively. A group of mice transferred with RORγt inhibitor–treated Th17 were administered with anti–IL-10R mAb (25 mg/kg) i.p. weekly. The other two groups of mice, which received control or RORγt inhibitor–treated Th17 cells, were given with anti-IgG Ab as controls. Five weeks after cell transfer, the severity of intestinal inflammation was assessed. (A) Colonic histopathology (original magnification × 100) and (B) histological scores are shown. (C) Colonic tissues were cultured in the medium for 24 h, and cytokine production in supernatants was assessed by ELISA. Data are shown as mean ± SD of 12 mice samples pooled from two experiments. *p < 0.05,**p < 0.01.
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