T Cells and Regulated Cell Death

Abstract

Cell death plays two major complementary roles in T cell biology: mediating the removal of cells that are targeted by T cells and the removal of T cells themselves. T cells serve as major actors in the adaptive immune response, and function by selectively killing cells which are infected or dysfunctional. The selectivity in the T cell recognition and elimination is a highly regulated feature, which in itself involves the death of both autoreactive T cells and T cells which are unable to recognise threats. Moreover, detection of potential threats will result in the activation and expansion of T cells, which upon resolution of the immune response will need to be eliminated. The culling of these T cells can be executed via a multitude of cell death pathways which are used in context-specific manners. Failure of these processes may result in an accumulation of misdirected or dysfunctional T cells, leading to complications such as autoimmunity or cancer. This review will focus on the role of cell death regulation in the maintenance of T-cell homeostasis as well as T cell-mediated elimination of infected or dysfunctional cells, and will summarize and discuss the current knowledge of the cellular mechanisms which are implicated in these processes.

A Hypoxia Gene-Based Signature to Predict the Survival and Affect the Tumor Immune Microenvironment of Osteosarcoma in Children

“…Hypoxia prevents T and NK cell development and activation in animal models [42]. Our analysis showed that children with osteosarcoma at high risk of experiencing hypoxia had an elevated number of CD4 cells, suggesting an immunosuppressive disorder.…”

Apoptosis Induction of Agave lechuguilla Torrey Extract on Human Lung Adenocarcinoma Cells (SK-LU-1)

“…By the intrinsic pathway of the mitochondria-dependent apoptosis, activation by the diflavonoid may be due to the fact that it is a stress promoter for the cell, which culminates in the mitochondrial outer membrane permeabilization (MOMP), allowing the release of proteins from the mitochondrial intermembrane space. This happens in T cells type II because the apoptotic signal needs to be amplified by caspases 3 and 7 [32,33]. In case the biflavonoid crosses the cell membrane, by active transport of K + /Na + pumps or even by the calcium–sodium ion exchanger, it can activate the signaling cascade of the binding with the Fas/CD95 receptor by the direct interaction of the biflavonoid with tBID through the R71 and S78 residues; however, BID (BH3 interacting-domain death agonist)is directly activated by caspase 8, generating a tBID, moving to the mitochondria to release cytochrome C (prior stimulation of the Bax–Bak complex, members of the pro-apoptotic Bcl-2 family) [32], to immediately form the caspase-9 Apaf1 complex, which activates caspase-6 and caspase-3 to induce apoptosis.…”

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