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. 2017 Nov 2;7:14940. doi: 10.1038/s41598-017-14780-4

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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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Palmitic acid-mediated ER stress suppresses IL-4 and IFN-γ production by iNKT cells via the IRE1α pathway. (a and b) iNKT cells were transfected with siRNA for control, Eif2ak3, Ern1, or Atf6 and treated with palmitic acid or vehicle in the presence of anti-CD3 and anti-CD28 mAbs for 24 h. (a) The efficiency of knockdown was estimated for each individual gene. (b) The levels of IL-4 and IFN-γ were measured in culture supernatants using ELISA. (c and d) iNKT cells were incubated with palmitic acid or vehicle in the presence of anti-CD3 and anti-CD28 mAbs for 24 h. To inhibit IRE1α, STF083010 was added during palmitic acid treatment. (c) The levels of cytosolic IL-4 and IFN- γ were estimated using cytometric analysis. (d) The transcription levels of t-bet and gata-3 were measured in the iNKT cell line using real time PCR, while the levels of IL-4 and IFN- γ were quantified using ELISA. *p < 0.05, **p < 0.01, ***p < 0.005.