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Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Immunol+Lett 2017 ; 184 (ä): 7-14 Nephropedia Template TP
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Inflammatory cytokines IL-17 and TNF-? up-regulate PD-L1 expression in human prostate and colon cancer cells #MMPMID28223102
Wang X; Yang L; Huang F; Zhang Q; Liu S; Ma L; You Z
Immunol Lett 2017[Apr]; 184 (ä): 7-14 PMID28223102show ga
Programmed cell death protein 1 (PD-1) acts on PD-1 ligands (PD-L1 and PD-L2) to suppress activation of cytotoxic T lymphocytes. Interleukin-17 (IL-17) and tumor necrosis factor-? (TNF-?) are co-expressed by T helper 17 (TH17) cells in many tumors. The purpose of this study was to test if IL-17 and TNF-? may synergistically induce PD-L1 expression in human prostate cancer LNCaP and human colon cancer HCT116 cell lines. We found that IL-17 did not induce PD-L1 mRNA expression, but up-regulated PD-L1 protein expression in HCT116 and LNCaP cells. TNF-? induced PD-L1 mRNA and protein expression in both cell lines. Neither IL-17 nor TNF-? induced PD-L2 mRNA or protein expression. IL-17 and TNF-? acted individually rather than cooperatively in induction of PD-L1 expression. IL-17 and/or TNF-? activated AKT, nuclear factor-?B (NF-?B), and extracellular signal-regulated kinases 1/2 (ERK1/2) signaling pathways in HCT116 cells, whereas only NF-?B signaling was activated in LNCaP cells. NF-?B inhibitor could diminish PD-L1 protein expression induced by IL-17 and/or TNF-? in both HCT116 and LNCaP cell lines. ERK1/2 inhibitor could also reduce PD-L1 protein expression induced by IL-17 and/or TNF-? in HCT116 cells, while AKT inhibitor could abolish PD-L1 protein expression induced by IL-17 and/or TNF-? in LNCaP cells. These results suggest that IL-17 and TNF-? act individually rather than cooperatively through activation of NF-?B and ERK1/2 signaling to up-regulate PD-L1 expression in HCT116 cells, while the two inflammatory cytokines act through activation of NF-?B signaling, in the presence of AKT activity, to up-regulate PD-L1 expression in LNCaP cells.