Cytotoxic T cells (CTLs) can kill target cells through two main mechanisms:
Perforin/Granzyme pathway – perforin forms pores and granzymes enter to trigger apoptosis.
Death receptor pathway – Fas ligand (FasL) on the CTL binds Fas (CD95) on the target cell, activating caspases and apoptosis.
👉 The Fas–FasL pathway does not cause TNF release. Instead, it directly activates apoptotic signaling in the target cell.
Where TNF (tumor necrosis factor, often TNF-α) comes in:
CTLs (and NK cells, and activated macrophages) can secrete TNF-α as part of their effector function.
TNF-α can bind TNFR1 on target cells, which may trigger apoptosis (through caspase-8) or promote survival/inflammation (through NF-κB), depending on the signaling context.
TNF is released by the immune effector cell, not by the dying target cell.