1. Vaginal CD11c+ DCs from IL-17A−/− mice are impaired in potentiating Th17 responses because of diminished IL-1β production.
Vaginal CD11c+ DCs from IL-17A−/− mice are impaired in potentiating Th17 responses because of diminished IL-1β production. Vaginal cells from hormone cycle–matched WT or IL-17A−/− mice (n = 5) were pooled, cultured overnight without any additional stimulation, stained with Abs against CD11c, CD11b, and IL-1β, and analyzed by flow cytometry to identify IL-1β+ cells, with dead cells excluded. (A) CD11c+ DCs were gated as shown, and (B) IL-1β expression by vaginal CD11c+ CD11b+ DCs from WT and IL-17A−/− mice was compared with isotype control. (C) The differences in percentage and (D) MFI of IL-1β+ DCs were compared between vaginal cells from WT and IL-17A−/− mice (n = 3 independent experiments). Data were analyzed using an unpaired t test with 95% confidence interval (*p < 0.05). (E) Vaginal cells from hormone cycle–matched WT or IL-17A−/− mice (n = 5) were pooled, pulsed with chicken OVA peptide, and cultured alone (TC) or cocultured at a 1:1 ratio with OT-II Tg CD4+ T cells (TC+CD4) for 3.5 d. Alternately, 100 ng/ml of rIL-1β was added on day 1 of coculture (TC+CD4+IL-1β). IL-17 levels in culture supernatants were measured by ELISA. Data are mean ± SEM of three individual wells per coculture condition. Data are representative of three independent experiments with similar results. Significance was calculated by two-way ANOVA (*p < 0.05, ***p < 0.001, ****p < ).
Varun C. Anipindi et al. ImmunoHorizons 2019;3:
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