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Journal ArticleDOI

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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Regulation of Alloreactive CD8 T Cell Responses by Costimulation and Inflammation

TL;DR: A novel murine anti-CD40 monoclonal antibody is described that prolongs skin allograft survival across major histocompatibility barriers and attenuates alloreactive CD8 T cell responses and it is found that the pro-apoptotic proteins Fas and Bim function concurrently to regulate peripheral tolerance induction to allografteds.
Journal ArticleDOI

Apoptosis and the Developing T Cells

TL;DR: The basic concepts involved in the extrinsic and intrinsic pathway of apoptosis are reviewed, and an overview of the events that leads immature T cells to survive or die by apoptosis during their intrathymic development are provided.
Journal ArticleDOI

Activation-dependent cell death of human monocytes is a novel mechanism of fine-tuning inflammation and autoimmunity.

TL;DR: The data suggest GM‐CSF/IFN‐γ induced cell death of monocytes as a novel mechanism to eliminate overactivated monocytes, thereby potentially balancing inflammation and autoimmunity in JIA.
Reference EntryDOI

Caspases in Inflammation and Immunity

TL;DR: The role of caspases in innate immunity is conserved through evolution, and the prototypical member of the inflammatory caspase subfamily, contributes to host defence through different interrelated mechanisms, notably cell repair, inflammation and cell death.
Journal ArticleDOI

Au-ACRAMTU-PEt3 Alters Redox Balance To Inhibit T Cell Proliferation and Function

TL;DR: Results demonstrate that Au-ACRAMTU-PEt3 has potent immunosuppressive activity that could be used to suppress immune responses during transplantation and autoimmunity.
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.
Journal ArticleDOI

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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