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Related Concept Videos

Complement System01:27

Complement System

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The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
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Inflammatory Response01:28

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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 JAK-STAT Signaling Pathway01:20

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
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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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Complement and inflammasome crosstalk in chronic inflammation.

Larisa Janžič1, Katarina Kouter1

  • 1Institute of microbiology and immunology, Faculty of medicine, University of Ljubljana, Ljubljana, Slovenia.

Frontiers in Immunology
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Summary

Chronic inflammation involves complex interactions between the complement system and inflammasomes, driving diseases like autoimmune disorders. Targeting these pathways offers new therapeutic strategies for persistent inflammation and tissue damage.

Keywords:
NLRP3chronic inflammationcomplement systeminflammasomesinnate immunity

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Area of Science:

  • Immunology
  • Innate Immunity
  • Chronic Inflammation

Background:

  • Chronic inflammation is a hallmark of numerous diseases, including autoimmune disorders, neurodegeneration, and metabolic syndromes.
  • The complement system and inflammasomes are key innate immune pathways that mediate inflammation.
  • These pathways are increasingly recognized for their interdependence in sustaining chronic inflammatory conditions.

Purpose of the Study:

  • To review the mechanistic crosstalk between complement activation and inflammasome signaling, focusing on the NLRP3 inflammasome.
  • To elucidate how these two systems interact to drive chronic inflammation and disease progression.
  • To explore potential therapeutic strategies targeting the complement-inflammasome axis.

Main Methods:

  • Review of existing literature on complement pathways, inflammasome signaling, and their interactions.
  • Analysis of shared activation triggers (e.g., ROS, mitochondrial damage) and feedback loops.
  • Examination of disease contexts where complement and inflammasome interplay is evident.

Main Results:

  • Complement activation drives inflammation via cell recruitment and cytokine induction.
  • NLRP3 inflammasome activation is sustained by diverse danger signals in chronic disease.
  • Mechanistic intersections include shared triggers, complement-mediated inflammasome priming/activation, and cytokine-driven feedback loops enhancing complement activity.

Conclusions:

  • Complement and inflammasomes form self-amplifying loops exacerbating inflammation and tissue damage in diseases like gout, atherosclerosis, and Alzheimer's.
  • Targeting these pathways, including dual-targeting approaches, shows clinical promise for immunomodulation.
  • Understanding this interplay is crucial for developing precise therapies for chronic inflammatory diseases.