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. 2019 Apr 5;9:5682. doi: 10.1038/s41598-019-41952-1

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© The Author(s) 2019

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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Anti-IFN-γ autoAbs block nitrite and chemokine production in monocytes and cytokine production during T cell activation. (a) Griess reaction showed the blockade of IFN-γ (10 ng/ml)-induced nitrite production by the indicated dilution of anti-IFN-γ autoAbs-contain patient sera (P1, P2, and P4), in human monocytic THP-1 cells incubated for 24 h. (b) ELISA showed the blockade of IFN-γ (10 ng/ml)-induced chemokine (IP-10 and MCP-1) production by 10³ dilution of anti-IFN-γ autoAbs-contain patient sera (P1, P2, and P4), in human monocytic THP-1 cells incubated for 24 h. (c) Data on IFN-γ, IL-2, and TNF-α production in anti-CD3/CD28 (0.5 μg/ml)-stimulated human Jurkat T cells incubated for 24 h. H, healthy control. The quantitative data are shown as mean ± SD of three independent experiments. ^**p < 0.01 and ^***p < 0.001, compared with untreated. ^#p < 0.05, ^##p < 0.01, and ^###p < 0.001, compared with H1.