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The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
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Antimicrobial proteins are important components of the immune system. They aid the body in combating pathogens by either killing them directly or hindering their replication processes. Four main types of antimicrobial substances are interferons, the complement system, iron-binding proteins, and antimicrobial proteins.
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Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
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Published on: May 21, 2018

Anthrax and the inflammasome.

Mahtab Moayeri1, Inka Sastalla, Stephen H Leppla

  • 1Laboratory of Bacterial Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. mmoayeri@niaid.nih.gov

Microbes and Infection
|December 31, 2011
PubMed
Summary
This summary is machine-generated.

Anthrax lethal toxin (LT) triggers Nlrp1 inflammasome activation in immune cells, leading to cell death and vascular collapse. This review details LT

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Area of Science:

  • Immunology
  • Toxicology
  • Cellular Biology

Background:

  • Anthrax lethal toxin (LT) is a critical factor in anthrax disease pathogenesis.
  • LT causes vascular collapse in susceptible animal models.
  • Nlrp1 inflammasome activation is implicated in LT's effects.

Purpose of the Study:

  • To review the mechanisms of Nlrp1 inflammasome activation by LT.
  • To discuss the cellular consequences of Nlrp1 activation.
  • To explore LT-induced effects in rodent models.

Main Methods:

  • Literature review of studies on anthrax lethal toxin and Nlrp1 inflammasome.
  • Analysis of cellular and animal models of anthrax toxin exposure.

Main Results:

  • LT activates the Nlrp1 inflammasome in macrophages and dendritic cells.
  • Activation leads to caspase-1, IL-1β, and IL-18 maturation.
  • This results in rapid cell death (pyroptosis) and contributes to disease.

Conclusions:

  • Nlrp1 inflammasome activation is a key cellular event in LT pathogenesis.
  • Understanding this pathway is crucial for developing countermeasures against anthrax.
  • Rodent models provide insights into toxin-mediated anthrax disease.