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Fig. 4 | Journal of Hematology & Oncology

Fig. 4

From: Th17 cells inhibit CD8+ T cell migration by systematically downregulating CXCR3 expression via IL-17A/STAT3 in advanced-stage colorectal cancer patients

Fig. 4

IL-17A inhibits CXCR3 expression on CD8+ T cells via STAT3 phosphorylation. a HD PB-derived CD8+ T cells were treated with rhIL-17A (20 ng/mL) for 48 h. Nuclei proteins were then subjected to multiplex profiling analysis for transcriptional factor activation. Activity was normalized with transcription factor IID and expressed as the relative light unit (RLU) of the transcriptional factor. b The upstream transcriptional factor of CXCR3 was identified via radar tools of the GCBI website. c The intersection of the screened transcriptional factors. Red circle: screened transcriptional factors (fold changes ≥ 4) from Fig. 4a; blue circle: upstream transcriptional factor of CXCR3 from Fig. 4b. d, e PBMCs from HDs (d) or purified CD8+ T cells (e) were treated with or without Stattic (10 nM). After 24 h and 48 h, CXCR3+CD8+ T cell expression was measured by flow cytometric analysis. Each line represented a different HD. f CXCR3+CD8+ T cell expression was measured after CD8+ T cells were treated with rhIL-17A (20 ng/mL) or Stattic (10 nM) for 48 h. g CD8+ T cells were incubated with rhIL-17A (5、10 and 20 ng/mL) for 48 h. P-STAT3 and CXCR3 expression levels were measured by western blotting. h CD8+ T cells were incubated with rhIL-17A (20 ng/mL) or Stattic (10 nM) for 48 h. i, j CXCR3+CD8+ T cell expression (i) or migratory ability of CD8+ T cells (j) was evaluated after treating sera collected from CRC patients (i) or RPMI-1640 conditional media (j) with rhIL-17A (20 ng/mL), anti-IL-17A (10 ng/mL), or Stattic. *P < 0.05, **P < 0.001

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