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Review
. 2010;2(4):316-24.
doi: 10.1159/000296915. Epub 2010 Mar 17.

Natural killer T cells and atherosclerosis: form and function meet pathogenesis

Nicole A Braun  1 , Roman Covarrubias, Amy S Major
Affiliations
Review

Natural killer T cells and atherosclerosis: form and function meet pathogenesis

Nicole A Braun et al. J Innate Immun. 2010.

Abstract

Atherosclerosis is a chronic inflammatory disease characterized by dyslipidemia and accumulation of lipids in the arterial intima, with activation of both innate and adaptive immunity. Reciprocally, dyslipidemia associated with atherosclerosis can perturb normal immune function. Natural killer T (NKT) cells are a specialized group of immune cells that share characteristics with both conventional T cells and natural killer cells. However, unlike these cells, NKT cells recognize glycolipid antigens and produce both pro- and anti-inflammatory cytokines upon activation. Because of these unique characteristics, NKT cells have recently been ascribed a role in the regulation of immunity and inflammation, including cardiovascular disease. In addition, NKT cells represent a bridge between dyslipidemia and immune regulation. This review summarizes the current knowledge of NKT cells and discusses the interplay between dyslipidemia and the normal functions of NKT cells and how this might modulate inflammation and atherosclerosis.

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Figures

Fig. 1
Fig. 1
iNKT cell receptor expression in comparison to NK cells and conventional CD4+ and CD8+ T cells.
Fig. 2
Fig. 2
Potential mechanisms of iNKT cell activation. a Direct activation of iNKT cells via exogenous glycolipids, such as α - GalCer, taken up by APCs and presented on CD1d. b Indirect activation of iNKT cells via TLR activation of APCs. Proinflammatory cytokines, such as IL-12, produced during APC activation, activate iNKT cells in combination with weak interactions of the iNKT cells with endogenous antigens.
See this image and copyright information in PMC

References

    1. Epstein SE, Zhu J, Burnett MS, Zhou YF, Vercellotti G, Hajjar D. Infection and atherosclerosis: potential roles of pathogen burden and molecular mimicry. Arterioscler Thromb Vasc Biol. 2000;20:1417–1420. - PubMed
    1. Farrugia PM, Lucariello R, Coppola JT. Human immunodeficiency virus and atherosclerosis. Cardiol Rev. 2009;17:211–215. - PubMed
    1. Matsuura E, Kobayashi K, Lopez LR. Atherosclerosis in autoimmune diseases. Curr Rheumatol Rep. 2009;11:61–69. - PubMed
    1. Van Oosten M, Rensen PC, Van Amersfoort ES, Van Eck M, Van Dam AM, Breve JJ, Vogel T, Panet A, Van Berkel TJ, Kuiper J. Apolipoprotein E protects against bacterial lipopolysaccharide-induced lethality. A new therapeutic approach to treat gram-negative sepsis. J Biol Chem. 2001;276:8820–8824. - PubMed
    1. Hyka N, Dayer J-M, Modoux C, Kohno T, Edwards CK, Roux-Lombard P, Burger D. Apolipoprotein A-I inhibits the production of interleukin 1b and tumor necrosis factor-α by blocking contact-mediated activation of monocytes by T lymphocytes. Blood. 2001;97:2381–2389. - PubMed

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