Research Paper Volume 12, Issue 1 pp 502—517

CXCL9 chemokine promotes the progression of human pancreatic adenocarcinoma through STAT3-dependent cytotoxic T lymphocyte suppression

Figure 6. STAT3 activation was responsible for the CXCL9-induced suppression of CD8+ T cell activation. (A) showed that CXCL9 dose-dependently induces activation of STAT3 and Ras signalling in CD8+ cytotoxic T cells; (B) showed that CXCL9 treatment could induce STAT3 activity in PAAD tumour; (C) showed that inhibition of STAT3 by selective inhibitor recovered CXCL9-suppressed division of CD8+ cytotoxic T cells; (D) inhibition of STAT3 by selective inhibitor attenuated the suppression of Ki67 expression in CXCL9-treated CD8+ cytotoxic T cells; (E) inhibition of STAT3 by selective inhibitor attenuated the suppression of Granzyme B expression in CXCL9-treated CD8+ cytotoxic T cells; (F) inhibition of STAT3 by selective inhibitor recovered the mRNA expression of anti-tumour cytokines IL2, TNFα and IFNγ in CD8+ cytotoxic T cells; (G) showed that inhibition of STAT3 by selective inhibitor recovered the secretion of anti-tumour cytokines IL2, TNFα and IFNγ in CD8+ cytotoxic T cells. *p<0.05, **p<0.01, ***p<0.001 when compared with CXCL9 treatment only. (H) showed that presence of STAT3 selective inhibitor could signficantly reduce the tumour burden in mice; (I) showed that tumour growth induced by CXCL9 was abolished by STAT3 selective inhibitor; (J) showed that enlarged tumour weight induced by CXCL9 was abolished by STAT3 selective inhibitor; (K) showed that presence of STAT3 selective inhibitor could recover the CD8+ population in PAAD tumour.