Cross-talk between tumor cells and neutrophils through the Fas (APO-1, CD95)/FasL system: Human glioma cells enhance cell viability and stimulate cytokine production in neutrophils

Wei Shio Hor, Wei Lune Huang, Yee Shin Lin, Bei Chang Yang

研究成果: Article同行評審

25 引文 斯高帕斯(Scopus)

摘要

Many tumor cells are resistant to Fas-mediated killing, which has been primarily used as a mechanism to evade immune attack. In this study, we found a new action of Fas on tumors where activation of the Fas signal may force tumor cells to produce survival factors for neutrophils. Human peripheral circulating neutrophils in coculture with glioma cells showed significant delays in spontaneous apoptosis. Interleukin (IL)-6 and IL-8 partially mediated the glioma cell-associated, protective effect on neutrophils. The Fas agonistic antibody CH-11 dose-dependently stimulated the expression of IL-6 and IL-8 in glioma cells. Accordingly, blocking the Fas/FasL interaction reduced IL-6 and IL-8 production in glioma cells and impaired their protective effect on neutrophils. Coculture with glioma cells also affected the expression of cytokines in neutrophils, including IL-8, interferon-γ, and tumor necrosis factor α to various extents. Collectively, our results demonstrate bi-directional cross-talk between tumor and immune cells. Although Fas activation alone cannot induce apoptosis in tumor cells, it may potentially initiate an effective anti-tumor response through a circumvented mechanism.

原文English
頁(從 - 到)363-368
頁數6
期刊Journal of Leukocyte Biology
73
發行號3
DOIs
出版狀態Published - 2003 3月 1

All Science Journal Classification (ASJC) codes

  • 免疫學和過敏
  • 免疫學
  • 細胞生物學

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