Arsenic induces tumor necrosis factor α release and tumor necrosis factor receptor 1 signaling in T helper cell apoptosis

JOURNAL OF INVESTIGATIVE DERMATOLOGY

卷:119

Article

Yu, HS ; Liao, WT ; Chang, KL ; Yu, CL ; Chen, GS

关键词: cytokine;    cytokine receptor;    cytotoxicity;    lymphocytes;    sodium arsenite;   

DOI  :  10.1046/j.1523-1747.2002.00475.x

来源: Elsevier

【 摘 要 】

Long-term exposure to arsenic induces arsenical cancers in human beings. Arsenic has been shown to induce apoptosis in a variety of cell systems. Previous studies revealed that patients with arsenic-induced Bowen's disease showed a defective cell-mediated immunity and decreased percentages of T cell and T helper cell subpopulations in peripheral mononuclear cells. The purpose of this study was to investigate the effects of arsenic on T cell survival and function in mononuclear cells. Arsenic concentrations higher than 1 muM induced tumor necrosis factor alpha release from mononuclear cells and caused a cytotoxic effect on T cells. When exposed to higher concentrations of arsenic, apoptosis was induced. CD4+ cells were the major apoptoic population in mononuclear cells. Tumor necrosis factor receptor 1 expression on CD4+ cells, but not Fas/FasL, was significantly enhanced by arsenic treatment compared to other mononuclear cells. Increased expressions of tumor necrosis factor receptor 1 related death domain proteins and activated caspases were observed. These findings indicate that tumor necrosis factor receptor 1 signaling is the major pathway in arsenic-induced T helper cell apoptosis.

【 授权许可】

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