T cells in atherogenesis: for better or for worse?
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.
Robertson
Anna-Karin L
AK
Section of Immunobiology and Howard Hughes Medical Institute, Yale School of Medicine, Immunobiology TAC S-560, PO Box 208011, New Haven, CT 06520, USA. anna-karin.robertson@yale.edu
Hansson
Göran K
GK
D000818:Animals; D000938:Antigen-Presenting Cells / Q000276:immunology; D000941:Antigens / Q000276:immunology; D015703:Antigens, CD / Q000276:immunology; D050197:Atherosclerosis / Q000276:immunology*; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D006801:Humans; D007109:Immunity; D013601:T-Lymphocytes / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology / Q000378:metabolism; D018418:Th2 Cells / Q000276:immunology / Q000378:metabolism
D000941:Antigens; D015703:Antigens, CD; D016207:Cytokines