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. 2013 Jan 22;110(6):2270–2275. doi: 10.1073/pnas.1206048110

Fig. 3.

Fig. 3.

MyD88-dependent IL-23R expression contributes to IL-17A production. (A) Purified CD4+ T cells were activated and cultured in the presence of the indicated cytokines for 5 d. 5, 20, or 100 ng/mL of IL-23 was added to the culture. Il17a and Il23r mRNA expression was quantified by qRT-PCR. After normalization to Actb, mRNA levels of CD4+ T cells treated with TGF-β + IL-6 were used as a control. (B) Myd88−/− CD4+ T cells were transduced with retroviral vectors encoding IRES-Thy1.1 (murine stem cell virus) or IL-23R-IRES-Thy1.1 (IL-23R) and cultured for 5 d under Th0 or Th17 conditions. IL-17A production was analyzed by flow cytometry. (C) Myd88−/− CD4+ T cells were transduced with retroviruses expressing NGFR, WT MyD88-NGFR (MyD88), or mutant MyD88 (truncated TIR domain)-NGFR (TIR) and cultured under Th17 conditions for 5 d. NGFR+CD4+ T cells were sorted, and mRNA expression of Il17a and Il23r was quantified by qRT-PCR. After normalization to Actb, mRNA levels of NGFR-transduced CD4+ T cells were used as a control. *P < 0.05. Results are representative of two independent experiments (A and C) or three independent experiments (B).