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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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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 adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
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Although not a source of energy, cholesterol plays a significant role as a foundational structure for bile salts, steroid hormones, and vitamin D, as well as being a crucial component of plasma membranes. Approximately 15% of blood cholesterol is derived from our diet, with the remainder synthesized from acetyl CoA by the liver and intestines. Cholesterol is eliminated from the body through its conversion into bile salts, which are eventually discarded in the feces.
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T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
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Complement activation by cholesterol crystals triggers a subsequent cytokine response.

Nathalie Niyonzima1, Bente Halvorsen2, Bjørnar Sporsheim3

  • 1Centre of Molecular Inflammation Research, Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, 7491 Trondheim, Norway; MRC Centre for Transplantation, Division of Transplant Immunology and Mucosal Biology, King's College London, SE1 9RT London, UK.

Molecular Immunology
|October 4, 2016
PubMed
Summary

Cholesterol crystals trigger inflammation in atherosclerosis by activating the complement system. Inhibiting complement early may be more effective than targeting downstream cytokines like IL-1β for treating this cardiovascular disease.

Keywords:
AtherosclerosisCholesterol crystalsComplementInflammasomeInterleukin-1beta

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Area of Science:

  • Immunology
  • Cardiovascular Research
  • Inflammation Biology

Background:

  • Endogenous danger signals, like cholesterol crystals (CC), promote inflammation in atherosclerosis.
  • CC accumulation in vessel walls activates the innate immune system and complement pathways.

Purpose of the Study:

  • To investigate the role of complement activation in cholesterol crystal-induced inflammation.
  • To evaluate complement inhibition as a therapeutic strategy for atherosclerosis.

Main Methods:

  • Analysis of complement system activation by cholesterol crystals.
  • Assessment of downstream inflammatory pathways, including NLRP3 inflammasome and IL-1β production.
  • Evaluation of therapeutic potential of complement inhibitors and 2-hydroxypropyl-β-cyclodextrin.

Main Results:

  • Cholesterol crystals activate complement pathways (lectin and classical), leading to C3 and C5 cleavage and inflammatory mediator release (e.g., C5a).
  • Complement activation by CC promotes crosstalk with the NLRP3 inflammasome-caspase-1 pathway, resulting in IL-1β production.
  • Upstream complement inhibition may offer a more efficient therapeutic approach than downstream IL-1β neutralization.

Conclusions:

  • The complement system is a critical upstream mediator in atherosclerosis pathophysiology.
  • Targeting complement activation presents a promising therapeutic strategy for controlling atherosclerosis progression.