Fig 2: IL-17A acts in synergy with TNF to promote CCL20 production by IEC in the presence or the absence of HIV-1(A) Intestinal epithelial cells (IEC; HT29 cell line) were cultured in 48 well-plates until 80% confluence (150,000 cells/well). IEC were activated with TNF (10 ng/mL) and/or IL-17A (10 ng/mL) for 24 h.(B) IEC cells were cultured in 48 well-plates wells until 80% confluence and activated with TNF (10 ng/mL) and/or IL-17A (10 ng/mL) for 3h and then exposed to T/F THRO (HIVTHRO) HIV strain (50 ng/well) for 24 h. Levels of CCL20 (A and B, left panels) and IL-8 (A and B, right panels) were quantified in cell culture supernatants by ELISA 24 h post-stimulation with cytokines (A) and/or HIV exposure (B). Paired t Test evaluated the statistical differences. p values are indicated on the graphs. Results are mean ± SD from three independent experiments performed with HT-29 IEC.

Fig 3: Effect of IL-17 on primary human intestinal epithelial cellsPrimary human Primary human intestinal epithelial cells (phIEC) were cultured in 48 well-plates for 5 days until 90% confluence (150,000 cells/well). phIEC were activated with TNF (10 ng/mL) and/or IL-17A (10 ng/mL) for 24 h.(A–C) IEC cells were cultured in 48 well-plates wells until 80% confluence and activated with TNF (10 ng/mL) and/or IL-17A (10 ng/mL) for 24h. Levels of CCL20 were quantified in cell-culture supernatants by ELISA (mean ± SD values of experimental triplicates) (A) and ISG15 and IFIT1 mRNA expression were quantified by RT-PCR (mean value of RT-PCR duplicate measurements) (B and C).