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. 2018 Jan 29;8:1826. doi: 10.1038/s41598-018-20197-4

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© The Author(s) 2018

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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AHR mediates the effects of all four ligands on T cell and antibody responses to infection. Age-matched and sex-matched Ahr^−/− mice were treated with AHR ligands and infected with IAV, as in Fig. 1. MLN and serum were harvested on day 9 post infection, and MLN cells were stained for flow cytometry. T cell subsets were defined as in Figs 2–4, and virus-specific IgG levels were measured by ELISA. Graphs depict the (a) the percent body weight change relative to the day prior to infection for mice in all treatment groups, (b) number of virus-specific (D^bNP_366–374⁺) CD8⁺ T cells, (c) the relative amount of circulating anti-influenza IgG2a, (d) the percentage of TBet⁺CD4⁺ (Th1) cells, (e) the percentage of CD44^hiCXCR5⁺PD-1⁺ CD4⁺ (Tfh) cells, and (f) percentage of Tregs (Foxp3⁺CD25⁺CD4⁺). 5–8 mice were used per treatment group. All data are shown ± SEM.