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. Author manuscript; available in PMC: 2019 Nov 1.
Published in final edited form as: J Autoimmun. 2018 Aug 8;94:122–133. doi: 10.1016/j.jaut.2018.07.022

Fig. 5. Pharmacological inhibition of MDR1/MRP4 boosts UCB effects in human Th17-cells.

Fig. 5.

Mean ± SEM frequency of CD39+ (A) and FOXP3+ (B) lymphocytes within UCB, RTV or UCB plus RTV-treated Th17-cells (gated as CD4+IL17+ lymphocytes) from n=12 HS and n=10 Crohn’s disease patients. Untreated (vehicle) controls are also shown. (C) Mean ± SEM frequency of CD39+ and FOXP3+ lymphocytes within LPMC-derived Th17-cells isolated from non-inflamed and inflamed bioptic colonic areas (n=9 Crohn’s). Cells were exposed to the same treatments as in (A) and (B). (D) Mean ± SEM % inhibition of IL17 and IFNγ production by CD4+CD25 responders in the presence of untreated, UCB, RTV or UCB plus RTV-treated Th17-cells (n=8 HS and n=15 Crohn’s); (E) Mean ± SEM CD39 and (F) FOXP3 MFI of untreated and UCB, RTV or UCB plus RTV-treated Th17-cells under normoxic or hypoxic conditions (n=5 HS and n=5 Crohn’s).

Comparisons were made using one-way ANOVA or Kruskal-Wallis test, followed by Tukey’s or Dunn’s multiple comparison tests. *P≤0.05;**P≤0.01;***P≤0.001.