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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:2493.)
© 2007 American Heart Association, Inc.

Editorials

The Influence of the Regulatory T Lymphocytes on Atherosclerosis

Israel Gotsman; Rajat Gupta; Andrew H. Lichtman

From the Heart Institute (I.G.), Hadassah University Hospital, Jerusalem, Israel; the Department of Medicine (R.G.), Massachusetts General Hospital, Boston; and the Vascular Research Division (A.H.L.), Department of Pathology, Brigham and Women’s Hospital, and Harvard Medical School, Boston.

Correspondence to Andrew H. Lichtman, MD, PhD, Department of Pathology, Brigham and Women’s Hospital, 77 Avenue Louis Pasteur, NRB 752N, Boston, MA 02115. E-mail alichtman@rics.bwh.harvard.edu

Key Words: atherosclerosis • regulatory T cell • cytokines

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

Atherosclerosis is complex inflammatory disease of the arterial wall, in which T lymphocytes play a significant role.¹ Since the recognition that T lymphocytes are present in human atherosclerotic plaque nearly 2 decades ago,² research has focused on the functional importance of these cells in the atherosclerotic process. The majority of T lymphocytes in atherosclerotic lesions are CD4⁺ T-helper cells with a phenotype characteristic of the proinflammatory T-helper 1 (Th1) subset. These cells recognize specifically antigens that are produced in relative abundance in hypercholesterolemic individuals or in plaques including oxidatively modified LDL (Ox-LDL) and HSP60/65. The T cells are activated when macrophage or dendritic cells present these antigens to the T cells in plaques or lymphoid tissues. The Th1 cells produce inflammatory cytokines IFN-, tumor necrosis factor (TNF)-, and membrane CD40-ligand, which amplify the immune response through activation of macrophages, vascular smooth muscle cells, and endothelial cells.¹

See page 2691

Many mechanisms have evolved to maintain immunologic self-tolerance and to limit responses to foreign antigens. One of these mechanisms involves regulatory T cells (Treg) that actively suppress responses of effector T cells. The best- characterized Treg are the natural CD4⁺CD25⁺ Treg that mature in the thymus and comprise 5% to 10% of peripheral CD4⁺ T cells.³ Other surface markers expressed by Treg include CTLA-4 and GITR. FoxP3, a forkhead family transcription factor, is a lineage specification factor for Treg and plays a crucial role in their suppressive function.⁴ Natural Treg are generated during thymic development, but Treg are . . . [Full Text of this Article]

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