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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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Caspase-8 activity has an essential role in CD95/Fas-mediated MAPK activation

TL;DR: The combination of biochemical analysis with mathematical modeling provides evidence for an important role of caspase-8 in CD95-mediated activation of MAPKs, while c-FLIP exerts a regulatory function in this process.
Journal ArticleDOI

Up-regulation of c-FLIPshort by NFAT contributes to apoptosis resistance of short-term activated T cells

TL;DR: It is shown that, in contrast to naive or long-termactivated T cells, short-term activated T cells strongly up-regulate the caspase-8 inhibitor, cellular FLICE-inhibitory protein (c-FLIP), and this implies that preventing autocrine CD95L signaling by c-FLip facilitates T-cell effector function and an efficient immune response.
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Defective thymopoiesis and poor peripheral homeostatic replenishment of T-helper cells cause T-cell lymphopenia in cirrhosis

TL;DR: Th-cell immunodeficiency in cirrhosis is explained by a universal defect in thymopoiesis exacerbated by splenic pooling and activation-driven cell-death induced by bacterial translocation.
Journal ArticleDOI

Dendritic Cells in Systemic Lupus Erythematosus: From Pathogenic Players to Therapeutic Tools

TL;DR: The current knowledge on the role of DC dysfunction in SLE pathogenesis is discussed, with the focus on DCs as targets for interventional therapies.
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Silencing of T lymphocytes by antigen-driven programmed death in recombinant adeno-associated virus vector–mediated gene therapy

TL;DR: Stable gene expression depended on selective death of CD8(+) T cells at the site of antigen production, an effective mechanism for subverting immunity that is also potentially reversible.
References
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Journal ArticleDOI

Caspases: Enemies Within

TL;DR: This work has shown that understanding caspase regulation is intimately linked to the ability to rationally manipulate apoptosis for therapeutic gain.
Journal ArticleDOI

Death receptors: signaling and modulation

Avi Ashkenazi, +1 more
- 28 Aug 1998 - 
TL;DR: Apoptosis is a cell suicide mechanism that enables metazoans to control cell number in tissues and to eliminate individual cells that threaten the animal's survival.
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Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death

TL;DR: In this article, the authors found that doubly deficient cells are resistant to multiple apoptotic stimuli that act through disruption of mitochondrial function: staurosporine, ultraviolet radiation, growth factor deprivation, etoposide, and the endoplasmic reticulum stress stimuli thapsigargin and tunicamycin.
Journal ArticleDOI

Signaling to NF-kappaB.

TL;DR: An overview of established NF-kappaB signaling pathways is provided with focus on the current state of research into the mechanisms that regulate IKK activation and NF- kappaB transcriptional activity.
Journal ArticleDOI

Missing Pieces in the NF-κB Puzzle

TL;DR: In this paper, a review of recent progress as well as unanswered questions regarding the regulation and function of NF-kappaB and IKK is presented, focusing on recent progress and unanswered questions.
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