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(Circulation Research. 2006;98:434.)
© 2006 American Heart Association, Inc.

Editorials

Antigen-Independent Targeting of Long-Lived CD4⁺ Cytolytic T Effector Cells to Lesions of Atherosclerosis

Elaine W. Raines

From the Department of Pathology, University of Washington, Seattle.

Correspondence to Elaine W. Raines, University of Washington, Department of Pathology, Harborview Medical Center, 325 Ninth Avenue, Box 359675, Seattle, WA 98104. E-mail ewraines@u.washington.edu

See related article, pages 524–531

Key Words: lymphoid • endothelial cell • smooth muscle cell • plaque stability • memory T cell • chemokine • xenograft

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

Acute coronary syndromes, most often characterized by fissuring or rupture of coronary lesions, are responsible for the majority of clinical manifestations of atherosclerosis.^1–3 Studies of human atherosclerotic plaques after acute events have revealed that lesions that tend to rupture are rich in inflammatory cells and have a thin fibrous cap, implicating the inflammatory response as a key regulator of plaque stability.^3–5 Activated inflammatory cells within lesions, particularly activated macrophages, have been considered to be prime candidates for regulating plaque stability by releasing matrix-degrading enzymes and apoptosis-inducing factors. Although CD4⁺ T cells are a recognized component of vulnerable plaques,⁵ studies have primarily focused on activities of their associated Th1 cytokines that cause activation of macrophages and other vascular cells.⁶ However, analysis of CD4⁺ T cells from patients with acute coronary syndrome have shown these T cells acquire unique properties including antigen-independent cytolytic capabilities that can kill endothelial cells and smooth muscle cells in vivo.^7–9 In this issue of Circulation Research, trafficking of these CD4 T effector cells into lesions is also shown to be independent of antigen stimulation,¹⁰ thus rendering them dangerous as they elude normal tolerance control.

Immune surveillance involves constant recirculation of lymphocytes through tissues. Naïve T cells traffic from the blood into the secondary lymphoid organs and then back into the blood via the afferent lymph, a cycle that continues until such time that they recognize antigens for which their T cell receptors are specific. Once activated, the T cells proliferate, generating short-lived effector cells that can . . . [Full Text of this Article]

Related Article:

Interleukin 12 Induces T-Cell Recruitment Into the Atherosclerotic Plaque

Xiaoyu Zhang, Alexander Niessner, Takako Nakajima, Wei Ma-Krupa, Stephen L. Kopecky, Robert L. Frye, Jörg J. Goronzy, and Cornelia M. Weyand
Circ. Res. 2006 98: 524-531. [Abstract] [Full Text] [PDF]

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