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. 2018 Oct 30;9:4515. doi: 10.1038/s41467-018-06924-5

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — HDAC2 inhibits IL-17 expression. a Knockdown of HDAC2 in cLPLs of WT mice using shRNA. ELISA was performed to measure IL-17A secretion in the culture supernatant of WT cLPLs treated with HDAC2-specific shRNA (shHDAC2) or control shRNA (shCtrl). b CD4⁺ T cells were isolated from WT and HDAC2^f/f CD4-Cre mice and were differentiated under Th17-inducing conditions. Real-time PCR and ELISA were performed to measure IL-17A expression. c Immunoblot analysis was performed to check the knockdown of ROR-γt in CD4⁺ T cells isolated from HDAC2^f/f CD4-Cre mice using ROR-γt-specific shRNA and differentiated under Th17-inducing conditions. d ELISA and e real-time PCR were performed to measure IL-17A expression in HDAC2^f/f CD4-Cre cells treated with ROR-γt-specific shRNA or control shRNA. f Schematic drawing of model shows that SUMOylation of ROR-γt facilitates recruitment of HDAC2, which inhibits IL-17 expression. Data are from one experiment representative of three or more independent experiments with similar results. *p < 0.05 and **p < 0.01, ns non-significant (two-tail t test) error bars are S.D.