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. 2017 Apr 21;7:1005. doi: 10.1038/s41598-017-00691-x

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© The Author(s) 2017

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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NOD1 silencing promotes il10 and march1 expression and decreases CD86 and IL-12 levels. (a/b) Immature DCs were generated and transfected with a control siRNA or siRNA directed against NOD1 (a) or NOD2 (b). 72 hours post transfection, cells were analysed for silencing efficiency or stimulated with IL-10 (30 ng/ml), and IL-10 target gene expression was monitored 2 hours post IL-10 induction. Data represent mean and SD of at least four independent experiments. (c) After 3 days of control or NOD1 silencing, DCs were induced with IL-10 for 4 hours. Cells were re-plated and cultured in fresh medium without IL-10 for 48 hours. IL-10 secretion was analysed after 48 hours by ELISA. Data represent mean and SD of four independent experiments. (d) 48 hours post IL-10 stimulation, CD86 expression and IL-12 secretion of control or NOD1 silenced DCs were evaluated by flow cytometry and ELISA, respectively. Data represent mean and SD of at least five independent experiments. For statistical analysis a one-way ANOVA with Tukey’s post hoc test was performed.