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Caspases01:24

Caspases

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Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
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Inflammatory Response01:28

Inflammatory Response

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An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
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The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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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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The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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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 of the Innate Immune Response01:28

Cells of the Innate Immune Response

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The innate immune response is an immediate and non-specific response against pathogens, acting swiftly to prevent the spread of infections. The primary cells involved in this response are phagocytes and natural killer (NK) cells.
Phagocytes
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Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

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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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Visualization of Inflammatory Caspases Induced Proximity in Human Monocyte-Derived Macrophages
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Evasion and interference: intracellular pathogens modulate caspase-dependent inflammatory responses.

Mary K Stewart1, Brad T Cookson1,2

  • 1Department of Microbiology, University of Washington, Seattle, Washington 98195, USA.

Nature Reviews. Microbiology
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Summary
This summary is machine-generated.

Pathogens use diverse strategies to evade host defenses, like altering lipopolysaccharide (LPS) structures and inhibiting inflammasome activation. Understanding these evasion tactics is key to controlling infections and inflammation.

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Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Pathogens interact with host surveillance systems for virulence.
  • Intracellular detection triggers pro-inflammatory caspase responses.

Purpose of the Study:

  • To review pathogen strategies for evading intracellular detection.
  • To discuss how pathogens inhibit caspase-dependent inflammatory responses.

Main Methods:

  • Review of scientific literature on pathogen-host interactions.
  • Analysis of molecular mechanisms used by bacteria and viruses.
  • Examination of immune evasion tactics.

Main Results:

  • Pathogens alter lipopolysaccharide (LPS) structures to evade detection.
  • Type III secretion systems are regulated to inhibit host responses.
  • Pathogens utilize proteins to block inflammasome formation and caspase activity.

Conclusions:

  • Pathogen evasion strategies target key intracellular surveillance pathways.
  • Regulation of inflammatory caspase activation is critical for host defense.
  • Modulating the inflammatory threshold balances infection resistance and host damage.