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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:e40.)
© 2005 American Heart Association, Inc.

Letters to the Editor

Natural Killer T Cells in Atherosclerosis

Yuri V. Bobryshev

Surgical Professorial Unit, St Vincent’s Hospital, Sydney, Australia

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

Natural Killer T (NKT) cells comprise a heterogeneous subpopulation of T cells that coexpress T cell receptor (TCR) and Natural Killer (NK) surface antigen CD161 in humans and NK1.1 in mice.^1,2 NKT cells are CD1d-restricted and express an evolutionary conserved TCR with invariant -chain (V14-J18 in mouse and V24-J18 in human).^1,2 NKT cells react to exogenous -galactosylceramide (GalCer), which is presented by monomorphic HLA class-I–like molecule CD1d.^1,2 It has been shown also that, in humans, some conventional T cells might upregulate NK receptors on activation.²

A number of recent experimental studies using mouse models have indicated a proatherogenic role of CD1d-restricted NKT cells in atherogenesis.^3–5 These works prompted us to examine whether T cells expressing perforin (CD161) are present in human atherosclerotic lesions.⁶ We found that, although small numbers of perforin-expressing T cells (CD161⁺CD3⁺) were present in all types of human atherosclerotic lesions, perforin-expressing T cells were most frequent in rupture-prone regions of advanced atherosclerotic plaques where perforin-expressing T cells constituted up to 2% of the total T cell population.⁵ Direct contacts of CD1d⁺ dendritic cells^7,8 with perforin-expressing T cells were observed in plaque rupture-prone regions,⁶ suggesting that dendritic cells may be involved locally in the regulation of perforin-expressing T cells.

In a very recent work, Aslanian et al⁹ examined the role of NKT cells in experimental atherosclerosis, comparing lesion size between CD1d^–/–LDLR^–/– and CD1d^+/+LDLR^–/– after 4, 8, and 12 weeks of feeding on a Western diet. The . . . [Full Text of this Article]

Israel F. Charo; Ara M. Aslanian

Gladstone Institute of Cardiovascular Disease, University of California, San Francisco