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Complement System01:27

Complement System

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 membrane...
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Screening Bioactive Nanoparticles in Phagocytic Immune Cells for Inhibitors of Toll-like Receptor Signaling
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Published on: July 26, 2017

Crosstalk between complement and toll-like receptors.

Wen-Chao Song1

  • 1Institute for Translational Medicine and Therapeutics and Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA. songwe@upenn.edu

Toxicologic Pathology
|November 24, 2011
PubMed
Summary
This summary is machine-generated.

The complement system and toll-like receptors (TLRs) work together in innate immunity. Their interaction amplifies inflammatory responses, offering new therapeutic targets for diseases like sepsis and autoimmune disorders.

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Area of Science:

  • Immunology
  • Innate Immunity

Background:

  • The complement system and toll-like receptors (TLRs) are key components of innate immunity.
  • Pathogen-associated molecular patterns often activate both systems simultaneously.

Purpose of the Study:

  • To investigate the synergistic interaction between the complement system and TLRs.
  • To understand the regulatory role of complement in TLR signaling.

Main Methods:

  • Studies in animal models, specifically mice deficient in a membrane complement regulator.
  • Analysis of systemic complement activation and proinflammatory cytokine biosynthesis following TLR ligand stimulation.

Main Results:

  • TLR ligand administration in complement-deficient mice led to increased complement activation and elevated proinflammatory cytokine production.
  • This synergistic effect required the interaction between complement and TLRs, as complement activation alone did not induce significant cytokine production.
  • Complement-mediated regulation of TLR signaling involved anaphylatoxins C5a and C3a, enhancing MAPK and NF-κB activation.

Conclusions:

  • A significant synergistic interaction exists between the complement system and TLRs, amplifying innate immune responses.
  • This crosstalk impacts adaptive immunity, including T helper 17 cell differentiation.
  • Understanding this interaction offers potential therapeutic strategies for inflammatory diseases.