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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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Autophagy01:27

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Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
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Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
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Eukaryotic cells use different mechanisms to eliminate toxic waste obsolete and worn-out substances. Lysosomes play a pivotal role in this, and hence, these substances are carried to the lysosome from other parts of the cell and extracellular space through different pathways. The most elaborately studied pathways to the lysosome are the endocytic pathways.
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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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Immune surveillance is an integral part of the innate immune system, involving the continuous monitoring of peripheral tissues to detect and respond to pathogens, infected cells, or cancerous cells. This surveillance is conducted primarily by natural killer (NK) cells and phagocytes, which employ distinct but complementary mechanisms to identify and eliminate threats.
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Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
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Autophagy and inflammasomes.

James Harris1, Tali Lang1, Jacinta P W Thomas1

  • 1Department of Medicine, School of Clinical Sciences at Monash Health, Monash University, Clayton, Victoria, Australia.

Molecular Immunology
|March 3, 2017
PubMed
Summary
This summary is machine-generated.

Autophagy, a cellular recycling process, is crucial for immune responses by regulating inflammasome activation and the release of inflammatory cytokines like IL-1β.

Keywords:
AIM2ASCAutophagosomesCaspase-1CytokinesIL-1MIFNLRP3

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Area of Science:

  • Cellular Biology
  • Immunology
  • Molecular Biology

Background:

  • Autophagy is a fundamental cellular process for degrading damaged components.
  • It plays vital roles in immunity, including antigen presentation and pathogen clearance.
  • Autophagy is implicated in regulating inflammatory responses.

Purpose of the Study:

  • To review the literature on autophagy's role in inflammasome activation.
  • To elucidate how autophagy influences the release of IL-1 family cytokines.

Main Methods:

  • Literature review of scientific articles.
  • Analysis of studies investigating autophagy and inflammasome pathways.
  • Synthesis of findings on IL-1β regulation by autophagy.

Main Results:

  • Autophagy regulates inflammasome activation through various mechanisms.
  • It removes inflammasome-activating signals and components.
  • Autophagy influences the fate and release of IL-1β.

Conclusions:

  • Autophagy is a critical regulator of inflammasome activation.
  • It significantly impacts the release of IL-1 family cytokines.
  • Understanding this interplay is key for immune system research.