Figure 4
Figure 4. Th17 cells induce Th1-type chemokines. (A-B) The correlations between IL-17 and Th1-type chemokines CXCL9 and CXCL10 in ovarian cancer ascites. IL-17, CXCL9, and CXCL10 were detected by ELISA in ovarian cancer ascites. The correlations between IL-17 and CXCL9 (A), and CXCL10 (B) were analyzed. (C-D) IL-17 and IFN-γ synergistically induced CXCL9 and CXCL10 production by primary ovarian tumor cells. Primary ovarian cancer cells (OC8) were cultured with IL-17 in the presence of variable concentrations of IFN-γ. CXCL9 and CXCL10 were detected in the cell supernatants by ELISA. Results are expressed as the mean values ± SEM (P < .05). (E) Th17 cells induced CXCL10 production by primary ovarian tumor cells through IL-17 and IFN-γ. Primary ovarian cancer cells were cultured with Th17-derived supernatants in the presence or absence of anti–IFN-γ and anti–IL-17. CXCL10 was detected in the cell supernatants by ELISA. Results are expressed as the mean values ± SEM (P < .05).

Th17 cells induce Th1-type chemokines. (A-B) The correlations between IL-17 and Th1-type chemokines CXCL9 and CXCL10 in ovarian cancer ascites. IL-17, CXCL9, and CXCL10 were detected by ELISA in ovarian cancer ascites. The correlations between IL-17 and CXCL9 (A), and CXCL10 (B) were analyzed. (C-D) IL-17 and IFN-γ synergistically induced CXCL9 and CXCL10 production by primary ovarian tumor cells. Primary ovarian cancer cells (OC8) were cultured with IL-17 in the presence of variable concentrations of IFN-γ. CXCL9 and CXCL10 were detected in the cell supernatants by ELISA. Results are expressed as the mean values ± SEM (P < .05). (E) Th17 cells induced CXCL10 production by primary ovarian tumor cells through IL-17 and IFN-γ. Primary ovarian cancer cells were cultured with Th17-derived supernatants in the presence or absence of anti–IFN-γ and anti–IL-17. CXCL10 was detected in the cell supernatants by ELISA. Results are expressed as the mean values ± SEM (P < .05).

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