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(Journal of Leukocyte Biology. 2003;73:363-368.)
© 2003 by Society for Leukocyte Biology

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 and Bei-Chang Yang

Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan, Taiwan

Correspondence: Bei-Chang Yang, Ph.D., Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan. E-mail: y1357{at}mail.ncku.edu.tw

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-{gamma}, and tumor necrosis factor {alpha} 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.

Key Words: apoptosis • IL-6 • IL-8




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