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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:1251.)
© 2002 American Heart Association, Inc.

Editorials

Do Natural Killer Cells Participate in a Killer Vascular Disease?

Godfrey S. Getz

From the Department of Pathology, University of Chicago, Ill.

Correspondence to Dr Godfrey S. Getz, University of Chicago, Department of Pathology, 5841 South Mayfield Ave, BH-329, MC 3083, Chicago, IL 60637-1470. E-mail g-getz@uchicago.edu

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

The article reporting on the exacerbated atherosclerosis in the double mutant, Lyst^beige, LDL receptor (LDLR) knockout is important in drawing attention to the possible involvement of natural killer (NK) cells in atherogenesis.¹ It is appropriate that NK cells come into focus: a recent review on immune mechanisms in atherosclerosis made scant mention of NK cells,² and they are important cytolytic cells of the innate immune system. The Lyst beige mutation results in a defect in the cytolytic function of NK cells, and this was demonstrated in the double mutant after consumption of a high-fat diet for 16 weeks.

See page 1341

So the authors asked whether the impaired cytolytic activity of NK cells in beige mice may account for the increased atherosclerosis they observed in these mice. To test this, they generated a second complex knockout mouse, one lacking both the LDLR and the perforin gene involved in the cytolytic activity of both cytotoxic T cells, NK T cells, and NK cells. The absence of the perforin gene had no effect on atherosclerosis, even though the total serum cholesterol was increased in these double knockout mice at 16 weeks of diet treatment.

Thus the cytolytic defect of NK cells in the Lyst beige LDLR-/- strain does not by itself seem to account for the increased atherosclerosis in this strain. NK cells are important components of the innate immune system. To ascertain whether the adaptive immune system might be implicated in the pro-atherogenic influence of the beige mutation, these experiments . . . [Full Text of this Article]

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