Caspases and T lymphocytes: a flip of the coin?

Abstract

In this review, we consider the role caspases play in cell death downstream of death receptors and cell intrinsic death mechanisms. In particular, we focus on these mechanisms in antigen-induced cell death, a mechanism which regulates the number of surviving T cells at the end of an immune response. The relative role of the apoptosome as an amplifier rather than an initiator of apoptosis is considered. Several factors that regulate the susceptibility to activation-induced cell death are considered. These factors emanate from the stimulation of the T-cell receptors and include multiple pathways. Recent work has shown that death receptor signaling can play an interesting role in cell proliferation in both humans and animals. These recent findings are discussed in the light of models of death receptor signaling.

Partial Cleavage of RasGAP by Caspases Is Required for Cell Survival in Mild Stress Conditions

“…Several inhibitors of caspases, such as cellular FLIPs and members of the IAP family, are potential candidates. FLIPs specifically prevent the activation of caspase 8 in response to Fas ligand or tumor necrosis factor but appear not to be involved in the regulation of other caspases (27). Consequently, it would not be anticipated that FLIPs protect cells once executioner caspases are activated.…”

T cell contributions to the different phases of granuloma formation

“…A full discussion of the complex pathways regulating cell survival, death and proliferation is beyond the scope of this review and the reader is referred to other recent reviews [45][46][47]. Increased expression of the death inducing Fas ligand (FasL) is detected in human leprosy and tuberculosis lesions [48].…”

Intrinsic and extrinsic control of effector T cell survival and memory T cell development

“…This causes release of cytochrome c into the cytoplasm, which integrates into a multi-subunit complex (the apoptosome) to activate the downstream eVector caspases 3 and 7 [6,17]. The disruption of the mitochondrial membrane is initiated by the expression and activation of BH3-only family proteins such as Bim, Bid, Bad, Puma, and Noxa, among others [6].…”