Fig. 1
IL-17 inhibits the infiltration of CD4+ T cells, and the production of TGF-β and IL-10 in CRC. a and b q-RT-PCR analyses of the indicated mRNAs in designated tissues of control and IL-17RA-deficient Cdx2-Cre+/ApcF/+ mice (a, n = 11), and Cdx2-Cre-ERT2+/ApcF/F mice (b, n = 5 for MLN, 11 for tumor). Mice in b received tamoxifen injection and were kept for 5 weeks for the development of early CRC tumors. Tumor-adjacent colonic tissues were used as “normal” control. c CD4+ T cells (CD45+ CD3+ CD4+), CD8+ T cells (CD45+ CD3+ CD8+), B cells (CD45+ CD19+), monocytes (CD45+ CD11b+ Ly-6CHigh), neutrophils (CD45+ CD11b+ Ly-6CLow, Ly-6G+), macrophages (CD45+ CD11b+, F4/80+), fibroblasts (CD45− EpCam−), and tumor cells (CD45− EpCam+) were FACS-sorted from pooled colonic tumors of 10 Il17ra+/+/Cdx2-Cre+/ApcF/+ mice. Purified cells were subjected to q-RT-PCR analysis, and the levels of each individual mRNA were shown as “1” in the cell type of highest expression. d Cdx2-Cre-ERT2+/ApcF/F mice that were Il17ra−/− or Il17ra+/− were given i.p. injection of tamoxifen (75 mg/kg body weight) daily for 3 consecutive days. Mice were sacrificed 5 weeks after tamoxifen-induced Apc ablation, and their mesenteric lymph nodes (MLN) and tumors were subjected to flow cytometry analysis. n = 5. Cells were isolated following collagenase digestion of the indicated tissues, followed by 4-h in vitro stimulation with PMA and ionomycin in the presence of Brefeldin A and monensin. e Representative flow cytometry plots for tumors samples from d. Data represent means ± S.E.M. *p < 0.05 in Students’ t test