Yu H.-S.Liao W.-T.Chang K.-L.CHIA-LI YUChen G.-S.2021-01-272021-01-2720020022-202Xhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-0036429952&doi=10.1046%2fj.1523-1747.2002.00475.x&partnerID=40&md5=6553075a7a67e28ddd3f632145af1832https://scholars.lib.ntu.edu.tw/handle/123456789/542241Long-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 μM induced tumor necrosis factor α 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.Cytokine; Cytokine receptor; Cytotoxicity; Lymphocytes; Sodium arsenite[SDGs]SDG3arsenic; caspase; Fas antigen; Fas ligand; tumor necrosis factor alpha; tumor necrosis factor receptor 1; adult; apoptosis; article; cell function; cell survival; controlled study; cytotoxicity; enzyme activation; helper cell; human; human cell; mononuclear cell; normal human; priority journal; protein domain; protein expression; protein induction; protein secretion; signal transduction; T lymphocytejournal article10.1046/j.1523-1747.2002.00475.x124063252-s2.0-0036429952