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Brief Reviews |
From Section of Immunobiology and Howard Hughes Medical Institute (A.-K.L.R.), Yale University School of Medicine, New Haven, Conn; Center for Molecular Medicine (G.K.H.), Department of Medicine, Karolinska Hospital, Karolinska Institute, Stockholm, Sweden.
Correspondence to Anna-Karin L Robertson, Yale School of Medicine, Immunobiology TAC S-560, PO Box 208011, New Haven, CT 06520. E-mail anna-karin.robertson{at}yale.edu
Series Editor: Göran K. Hansson Previous Brief Reviews in this Series:
Nilsson J, Hansson GK, Shad PK. Immunomodulation of atherosclerosis: implications for vaccine development. 2005;25:1828.
Frostegård J. Atherosclerosis in patients with autoimmune disorders. 2005;25:17761785.
The idea that atherosclerosis is an inflammatory disease is no longer controversial. Instead, much of the current research is now focused on understanding what drives this inflammation and how it is regulated. Adaptive immunity, in particular T cells, is highly involved in atherogenesis. It is well known that different subsets of T cells can drive or dampen inflammatory processes, but we still have much to learn about the regulation of this balance in the context of atherosclerosis. This review summarizes our knowledge of T cells in atherogenesis, their potential antigens, their contact-dependent activities, and their secretion of inflammatory and antiinflammatory mediators, aiming to illustrate how T cells can aggravate or attenuate this disease through cross-talk with other cells within or outside the atherosclerotic plaque.
Adaptive immunity, in particular T cells, is highly involved in the development of atherosclerosis. This review summarizes our current knowledge of T cells in atherogenesis and illustrates how they can aggravate or attenuate this disease through cross-talk with other cells within or outside the atherosclerotic plaque.
Key Words: atherosclerosis pathophysiology immune system T cells cytokines macrophages
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