Fig. 7

MCP230-induced pulmonary Th17 immune response is dependent on AHR activation. WT mice were exposed to vehicle or MCP230 (50 μg) that were treated with or without AHR antagonist (CH223191; 10 mg/kg) 2 h prior to the exposure. Lungs or BALF were collected at 5 dpe. (a, b) Lungs were used to determine adaptive T cell responses. PMA/ionomycin-stimulated lung cells were stained with surface (CD3 and CD4) and intracellular (IL17A) antibodies. T cell subsets were quantified using flow cytometry. Data are presented as percentage of IL17A⁺ cells among CD3⁺CD4⁺ cells (a) and representative flow cytometry pseudo color dot plots of IL17A⁺CD4⁺ cells gated on CD3⁺ T cells (b). Data represent mean ± SEM from 4 to 5 mice. ^ap < 0.05, compared to Vehicle group. ^bp < 0.05, compared to MCP230 group, one-way ANOVA with Holm-Sidak’s multiple comparisons test. (c) BALF were used to assess differential cell counts by counting at least 300 cells/sample. Data represent mean ± SEM from one of two independent experiments, 4 to 5 mice. ^ap < 0.05, compared to Vehicle group. ^bp < 0.05, compared to MCP230 group, one-way ANOVA with Dunnett’s multiple comparisons test