This study examined the effects of arsenic trioxide on apoptosis and interleukin-4 release in T cells of asthmatic patients in vitro and investigated the role of Bcl-2 in the active mechanism. T cells were isolated from asthmatic patients (n = 21) and healthy controls (n = 20), and then treated with arsenic trioxide and dexamethasone. Cell apoptosis was measured using fluorescence microscopy, flow cytometry and a cytochrome c ELISA kit. Interleukin-4 levels in the serum and in supernatants from T cells were quantified by ELISA. Flow cytometric analysis and immunofluorescence studies were performed to determine Bcl-2 expression. T cells of the asthmatic patients (i. e. without treatment) exhibited decelerated spontaneous apoptosis after 24 h incubation in vitro when compared to T cells of the healthy controls. With dexamethasone treatment, an increase in apoptosis of T cells was not significantly different between both groups, irrespective of the method used. Arsenic trioxide treatment, however, significantly increased the apoptosis of T cells of the asthmatic group and showed a slight effect on the control group. In asthmatic patients, elevated levels of interleukin-4 and up-regulated Bcl-2 expression were detected. Moreover, in vitro, T cells of asthmatic patients spontaneously released more interleukin-4 and exhibited more Bcl-2 expression than T cells from the control group. Arsenic trioxide treatment significantly decreased interleukin-4 release and down-regulated Bcl-2 expression in asthmatic patients, while it only slightly affected healthy controls. Dexamethasone treatment decreased interleukin-4 release in both groups examined. It did not significantly influence Bcl-2 expression. These results suggest that arsenic trioxide induces T cell apoptosis and decreases interleukin-4 release in T cells of asthmatic patients in vitro and that down-regulation of Bcl-2 expression may be an important mechanism.