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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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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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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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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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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
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Canonical Inflammasomes.

Vinicius Nunes Cordeiro Leal1, Alessandra Pontillo2

  • 1Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brasil.

Methods in Molecular Biology (Clifton, N.J.)
|August 14, 2023
PubMed
Summary

The innate immune system uses pattern recognition receptors (PRRs) to detect threats. Canonical inflammasomes, activated by PRRs, trigger caspase-1 to release inflammatory cytokines and induce pyroptosis.

Keywords:
Canonical activationInflammasomePRRs

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Area of Science:

  • Immunology
  • Cell Biology

Background:

  • The innate immune system is the host's primary defense against pathogens and cellular damage.
  • Pattern recognition receptors (PRRs) detect pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs).

Purpose of the Study:

  • To explain the activation mechanism of canonical inflammasomes.
  • To detail the role of inflammasomes in innate immunity and host defense.

Main Methods:

  • Review of literature on inflammasome activation pathways.
  • Description of key molecular players including NLRs, PYD-containing proteins, caspase-1, and gasdermin D.

Main Results:

  • Canonical inflammasomes are activated by specific PRRs, leading to caspase-1 activation.
  • Caspase-1 processes pro-inflammatory cytokines IL-1ß and IL-18, and gasdermin D.
  • Gasdermin D mediates cytokine release and induces pyroptosis, a form of inflammatory cell death.

Conclusions:

  • Canonical inflammasomes are crucial sensors of infection and homeostatic disturbances.
  • Inflammasome activation leads to potent inflammatory responses and cell death, critical for host defense.