Th17 cells known as Interleukin-17 (Inflammatory Cytokine) producing cells are differentiated subsets from naïve CD4+ T cells and have crucial roles in regulation of inflammation, host defense and autoimmunity. TCR (T Cell Receptor) activation is triggered under Th17 cell culture conditions and resulting naïve CD4+ T cells are induced to differentiate through Th17 cells. In the life time of activated T cells, the activation process also induces an apoptotic mechanism which is called activation-induced cell death (AICD) for elimination of activated cells from the environment for maintenance of homeostasis. AICD is known as the main programmed cell death mechanism for T cells by Fas-FasL signaling resulting activation of early and late apoptotic caspase proteins such as caspase-3 and caspase-8. Moreover, Interleukin-7, which is a member of Interleukin-2 family, has a survival mechanism in T cells by the activation and maintenance of anti-apoptotic proteins mainly Bcl-2 and inhibition of pro-apoptotic proteins such as Bax and Bim. This research analyzes apoptosis mechanism in Th17 cells in terms of AICD and the effects of IL-7 on that apoptosis signaling pathway. Our results showed that IL-7 did not have any effect to AICD throughout Fas-FasL signaling and activation of caspase-3 and caspase-8 protein.