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A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
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Killer cells in atherosclerosis.

Tin Kyaw1, Peter Tipping2, Ban-Hock Toh2

  • 1Baker Heart and Diabetes Institute, Melbourne, Australia; Centre for Inflammatory Diseases, Department of Medicine, Monash University, Melbourne, Australia.

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|May 10, 2017
PubMed
Summary
This summary is machine-generated.

Cytotoxic lymphocytes, or killer cells, contribute to cell death in atherosclerotic lesions, potentially causing plaque rupture. Therapies targeting these cells may prevent heart attacks and strokes while preserving immune function.

Keywords:
AtherosclerosisCell deathCytotoxicityKiller cellsUnstable plaque

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Area of Science:

  • Immunology
  • Cardiovascular Disease Research

Background:

  • Cytotoxic lymphocytes (killer cells) are crucial for immunity and tumor surveillance but can harm tissues in chronic inflammation and autoimmune diseases.
  • Cell death and necrosis are hallmarks of advanced atherosclerotic lesions, particularly vulnerable plaques linked to heart attacks and strokes.

Purpose of the Study:

  • To review the role of killer cells in atherosclerosis, including their types, activation, migration, and effector functions.
  • To discuss therapeutic strategies targeting killer cells in atherosclerotic lesions.

Main Methods:

  • Review of current scientific literature on killer cells in atherosclerosis.
  • Examination of cytotoxic mechanisms employed by killer cells.
  • Analysis of adaptive and innate killer cell subsets (CD8 T cells, CD28- CD4 T cells, NK cells, γδ-T cells).

Main Results:

  • Accumulation of killer cells in human and mouse atherosclerotic lesions suggests their contribution to lesion progression and instability.
  • Killer cells induce target cell death via cytotoxic mechanisms like perforin, granzymes, TRAIL, FasL, and TNF-α.
  • Specific killer cell subsets are implicated in the pathogenesis of atherosclerosis.

Conclusions:

  • Killer cells are key players in atherosclerotic plaque development and rupture.
  • Targeting killer cell cytotoxicity within lesions offers a therapeutic avenue for cardiovascular disease.
  • Immunomodulatory therapies should selectively target lesion-resident killer cells to avoid systemic immune suppression.