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. 2019 Oct 14;9:14766. doi: 10.1038/s41598-019-51311-9

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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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CCR4 induces Th1 polarization upon CVB5 infection. C57BL/6 and CCR4^−/− mice were infected with CVB5 (A–D). (A,B) The production of IFN-γ and IL-17 by CD4⁺ and CD8⁺ T cells was evaluated at day 7 post infection by flow cytometry after ex vivo stimulation with PMA and ionomycin in the presence of brefeldin-A. (C) IFN-γ and IL-17 were measured in the pancreas homogenate by ELISA at day 7. (D) C57BL/6 mice were treated on days −1, 1, 3 and 5 with anti-CCL17 antibody, and the expression of ifng and il17 was evaluated in the pancreas at 7 days post-infection. (E) Survival of C57BL/6 (WT), IFN-γ^−/− and IL-17^−/− mice after CVB5 infection. N = 5–10 mice per group. The data are shown as the means + SEM from at least 3 independent experiments, and * indicates p < 0.05.