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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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The Extrinsic Apoptotic Pathway01:17

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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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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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Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
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WildCARDs: inflammatory caspases directly detect LPS.

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Summary

A new study reveals inflammasomes are not the only pathway for inflammatory caspase activation. Caspase-4, -5, and -11 can directly bind to LPS, initiating auto-activation and cell death.

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Inflammasomes traditionally activate inflammatory caspases, primarily caspase-1.
  • This mechanism has been the established model for inflammatory caspase activation.

Purpose of the Study:

  • To investigate alternative pathways for inflammatory caspase activation.
  • To challenge the prevailing paradigm of inflammasome-centric caspase activation.

Main Methods:

  • The study by Shi et al. investigated the direct interaction of caspases with cytosolic LPS.
  • Analysis of caspase auto-activation and subsequent cell death pathways.

Main Results:

  • Caspase-4, -5, and -11 directly bind to cytosolic lipopolysaccharide (LPS).
  • This direct binding triggers auto-activation of these caspases.
  • Activation leads to pyroptotic cell death, independent of inflammasomes.

Conclusions:

  • A novel paradigm for inflammatory caspase activation has been identified.
  • Caspase-4, -5, and -11 represent a distinct pathway for initiating inflammation and cell death.
  • This discovery redefines our understanding of innate immune sensing and inflammatory responses.