Letter to the Editor

In Response:

The letter by Zal et al addresses an important issue. It is undisputed that CD4+CD28⁻ T cells can be clonally expanded in the periphery and that T cells belonging to these clones infiltrate into atherosclerotic plaques.¹ How much of their activity that is antigen specific, however, is still a question of debate. The Weyand group has shown that CD4+CD28⁻ T cells are able to lyse endothelial cells in vitro without the need for antigen recognition.² In addition, they have provided evidence that interleukin (IL)-12 enhances lesion recruitment of these cells.³ Weyand and colleagues state “Thus, (CD4+)CD28⁻ T cells functionally resemble NK cells, which have proinflammatory activity even in the unprimed state and respond to any IL-12–inducing host infection with a shift in tissue trafficking and accrual in inflammatory lesions”.³ At present, both antigen specific and unspecific activation of CD4+CD28⁻ T cells are therefore possible scenarios, and more studies are needed to shed light on this issue.

Consulting Editor for this article was Alan M. Fogelman, MD, Professor of Medicine and Executive Chair, Department of Medicine and Cardiology, UCLA School of Medicine, Los Angeles, Calif.