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Life and death in peripheral T cells

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TLDR
The concepts of activation-induced cell death (AICD) and activated cell-autonomous death (ACAD) in the regulation of life and death in T cells are discussed.
Abstract
During the course of an immune response, antigen-reactive T cells clonally expand and then are removed by apoptosis to maintain immune homeostasis. Life and death of T cells is determined by multiple factors, such as T-cell receptor triggering, co-stimulation or cytokine signalling, and by molecules, such as caspase-8 (FLICE)-like inhibitory protein (FLIP) and haematopoietic progenitor kinase 1 (HPK1), which regulate the nuclear factor-kappaB (NF-kappaB) pathway. Here, we discuss the concepts of activation-induced cell death (AICD) and activated cell-autonomous death (ACAD) in the regulation of life and death in T cells.

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Death receptor signal transducers: nodes of coordination in immune signaling networks.

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Nuclear factor-κB is a critical mediator of stress-impaired neurogenesis and depressive behavior

TL;DR: A critical role is demonstrated for NF-κB signaling in the actions of IL-1β and stress, which is identified as a critical mediator of the antineurogenic and behavioral actions of stress and suggests previously undescribed therapeutical targets for depression.
References
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Molecular mechanisms of activated T cell death in vivo

TL;DR: The culmination of the immune response involves the death of the majority of the activated antigen-specific T lymphocytes, and the mechanisms that control thedeath of these activated cells are focused on.
Journal ArticleDOI

Activation of NF-κB by FADD, Casper, and Caspase-8

TL;DR: It is shown that overexpression of FADD and Casper potently activates NF-κB, and that activated caspase-8 can negatively regulate TNF-R1-induced NF-KKB activation by proteolytically inactivating NIK.
Journal ArticleDOI

cFLIP regulation of lymphocyte activation and development

TL;DR: Insight gained from studies indicates that cFLIP and caspase-8 form a heterodimer that ultimately links T-cell-receptor signalling to activation of nuclear factor-κB through a complex that includes B-cell lymphoma 10 (BCL-10), mucosa-associated-lymphoid-tissue lymphoma-translocation gene 1 (MALT1) and receptor-interacting protein 1 (RIP1).
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