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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:E18.)
© 2007 American Heart Association, Inc.

Letters to the Editor

Letter to the Editor

Autoreactive CD4⁺CD28^– T Cells and Acute Coronary Syndromes

Behnam Zal; Christina Baboonian; Juan Carlos Kaski

Department of Cardiac and Vascular Sciences, St. George’s University of London, UK

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

To the Editor:

The review article by Robertson and Hansson¹ on the role of T cells in atherogenesis is comprehensive and scholarly. A particular aspect of the problem, however, which in our view is of potential pathogenic relevance, has been only tangentially addressed in the article. Robertson and Hansson¹ mention that patients with acute coronary syndrome (ACS) may exhibit a peripheral burst of an unusual and aggressive CD4⁺ T cell subset that lacks the expression of the CD28 receptor (CD4⁺CD28^– cells). In these patients, CD4⁺CD28^– cells can represent up to 50% of the circulating CD4⁺ cell compartment, and are also preferentially recruited into culprit lesions.^2,3 CD4⁺CD28^– T cells, unlike typical CD4⁺cells, produce high levels of interferon (INF) (INF)-, interleukin (IL)-2, and cytotoxic perforin granules.³ The potent proinflammatory and cytolytic properties of these T cells are considered to be important factors contributing to atheromatous plaque destabilization.^4,5

Robertson and Hansson¹ suggest that the cytolytic function of CD4⁺CD28^– cells against autologous cells may be nonspecific and therefore indiscriminate. Published data, however, indicate that this may not be the case, as the loss of CD28 cell surface expression and clonal outgrowth of these T cells is reported to be the result of their chronic exposure to a restricted spectrum of antigens,^6,7 which may be present in the atherosclerotic plaque and/or the peripheral circulation.³ Indeed, we have recently shown that circulating CD4⁺CD28^– cells in ACS patients are activated in response to a restricted antigenic stimulation.⁸ CD4⁺CD28^– cells . . . [Full Text of this Article]