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. 2021 Nov 13;18:265. doi: 10.1186/s12974-021-02316-7

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© The Author(s) 2021

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — Control of IL-17A production in γδ but not CD4⁺ T cells is dependent on IL-10R expression on Foxp3⁺ Tregs. A Flow cytometric analysis of the IL-10R (CD210) Mean Fluorescent Intensity (MFI) on Foxp3⁺ and Foxp3⁻ CD4⁺ T cells in FIR-tiger mice. Flow cytometric analysis of IL-17A produced by CD4⁺ (B) and γδ (C) T cells isolated from ischemic hemispheres of Foxp3^CreIl10Ra^wt/wt and Foxp3^CreIl10Ra^fl/fl controls 7 days after tMCAO. (D) Proposed mechanism of protection from ischemic brain injury induced by IL-10. Flow cytometric data is presented as mean ± SEM of 6 FIR-tiger (A) and 6 Foxp3^CreIl10Ra^wt/wt and 7 Foxp3^CreIl10Ra^fl/fl mice per group (B, C). Statistical significances were analyzed by Student t test (A–C). **P < 0.01 and ***P < 0.01