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Cardiovascular Research 2003 60(1):78-86; doi:10.1016/S0008-6363(03)00341-9
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

T lymphocytes in atherogenesis—functional aspects and antigenic repertoire

Onno J de Boer*, Anton E Becker and Allard C van der Wal

Department of Cardiovascular Pathology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands

*Corresponding author. Tel.: +31-20-566-4369; fax: +31-20-691-4738. Email address: o.j.deboer@amc.uva.nl

Received 13 December 2002; accepted 25 February 2003

KEYWORDS Atherosclerosis; Immunology; Infection/inflammation; T-cells; Cytokines

The first 150 words of the full text of this article appear below.


   1. Introduction
 
Atherosclerosis represents an inflammatory and reparative response to chronic or episodic injury of arterial intima [1]. During the longstanding process of plaque formation a myriad of secretory products of inflammatory cells is released in the plaque, likely connected to the nature and extent of injury to the vessel wall. These inflammatory mediators do not only have profound effects on growth and morphologic differentiation of plaques, but eventually may also initiate plaque rupture, and thus life threatening complications such as myocardial infarction and stroke [2]. Such insights have led to intense investigations over the past years tempting to unravel molecular and cellular basis of plaque inflammation, which include also factors that initiate or sustain the inflammatory response. Cell types that take part in plaque inflammation are macrophages, T-lymphocytes, mast cells and dendritic cells. Among these, the participation of T cells in atherogenesis is relevant for several reasons. First, T-cells . . . [Full Text of this Article]


   2. T-cell immune responses in atherosclerotic lesions
 
2.1. Basic aspects of T-cell immunity
2.2. Lymphocytes in various stages of plaque developments
2.3. Site of T-cell recruitment
2.4. T-cells and clinical manifestations of atherosclerosis

   3. T-cells and initiators of plaque inflammation
 
3.1. Antigen independent T-cell activation
3.2. Antigen specific T-cell activation

   4. Conclusions
 

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