Review |
From the Center for Molecular Medicine and Department of Medicine (G.K.H., Z.-Q.Y.), Karolinska Institute, Stockholm, Sweden; and Leducq Center for Cardiovascular Research (P.L., U.S.), Department of Medicine, Brigham and Womens Hospital, Harvard Medical School, Boston, Mass.
Correspondence to Dr Göran K Hansson, CMM L8:03, Karolinska Hospital, SE-17176 Stockholm, Sweden. E-mail Goran.Hansson@ cmm.ki.se
This review considers critically the evidence for the involvement of mediators of innate and acquired immunity in various stages of atherosclerosis. Rapidly mobilized arms of innate immunity, including phagocytic leukocytes, complement, and proinflammatory cytokines, contribute to atherogenesis. In addition, adaptive immunity, with its T cells, antibodies, and immunoregulatory cytokines, powerfully modulates disease activity and progression. Atherogenesis involves cross talk between and shared pathways involved in adaptive and innate immunity. Immune processes can influence the balance between cell proliferation and death, between synthetic and degradative processes, and between pro- and antithrombotic processes. Various established and emerging risk factors for atherosclerosis modulate aspects of immune responses, including lipoproteins and their modified products, vasoactive peptides, and infectious agents. As we fill in the molecular details, new potential targets for therapies will doubtless emerge.
Key Words: lymphocytes macrophages antibody inflammation cytokines
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Z. Liu, C. Zhang, N. Dronadula, Q. Li, and G. N. Rao Blockade of Nuclear Factor of Activated T Cells Activation Signaling Suppresses Balloon Injury-induced Neointima Formation in a Rat Carotid Artery Model J. Biol. Chem., April 15, 2005; 280(15): 14700 - 14708. [Abstract] [Full Text] [PDF] |
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Y. Michowitz, E. Goldstein, A. Roth, A. Afek, A. Abashidze, Y. Ben Gal, G. Keren, and J. George The involvement of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in atherosclerosis J. Am. Coll. Cardiol., April 5, 2005; 45(7): 1018 - 1024. [Abstract] [Full Text] [PDF] |
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C. Tenger, A. Sundborger, J. Jawien, and X. Zhou IL-18 Accelerates Atherosclerosis Accompanied by Elevation of IFN-{gamma} and CXCL16 Expression Independently of T Cells Arterioscler. Thromb. Vasc. Biol., April 1, 2005; 25(4): 791 - 796. [Abstract] [Full Text] [PDF] |
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S. L. Karackattu, M. H. Picard, and M. Krieger Lymphocytes Are Not Required for the Rapid Onset of Coronary Heart Disease in Scavenger Receptor Class B Type I/Apolipoprotein E Double Knockout Mice Arterioscler. Thromb. Vasc. Biol., April 1, 2005; 25(4): 803 - 808. [Abstract] [Full Text] [PDF] |
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W. L. Chan, N. Pejnovic, H. Hamilton, T. V. Liew, D. Popadic, A. Poggi, and S. M. Khan Atherosclerotic Abdominal Aortic Aneurysm and the Interaction Between Autologous Human Plaque-Derived Vascular Smooth Muscle Cells, Type 1 NKT, and Helper T Cells Circ. Res., April 1, 2005; 96(6): 675 - 683. [Abstract] [Full Text] [PDF] |
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X. Zhou, A.-K. L. Robertson, M. Rudling, P. Parini, and G. K. Hansson Lesion Development and Response to Immunization Reveal a Complex Role for CD4 in Atherosclerosis Circ. Res., March 4, 2005; 96(4): 427 - 434. [Abstract] [Full Text] [PDF] |
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A. Chait, C. Y. Han, J. F. Oram, and J. W. Heinecke Thematic review series: The Immune System and Atherogenesis. Lipoprotein-associated inflammatory proteins: markers or mediators of cardiovascular disease? J. Lipid Res., March 1, 2005; 46(3): 389 - 403. [Abstract] [Full Text] [PDF] |
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J. Rupp, T. Hellwig-Burgel, V. Wobbe, U. Seitzer, E. Brandt, and M. Maass Chlamydia pneumoniae infection promotes a proliferative phenotype in the vasculature through Egr-1 activation in vitro and in vivo PNAS, March 1, 2005; 102(9): 3447 - 3452. [Abstract] [Full Text] [PDF] |
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S.-X. Wang, P. K. Elder, Y. Zheng, A. R. Strauch, and R. J. Kelm Jr. Cell Cycle-mediated Regulation of Smooth Muscle {alpha}-Actin Gene Transcription in Fibroblasts and Vascular Smooth Muscle Cells Involves Multiple Adenovirus E1A-interacting Cofactors J. Biol. Chem., February 18, 2005; 280(7): 6204 - 6214. [Abstract] [Full Text] [PDF] |
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N. Dronadula, Z. Liu, C. Wang, H. Cao, and G. N. Rao STAT-3-dependent Cytosolic Phospholipase A2 Expression Is Required for Thrombin-induced Vascular Smooth Muscle Cell Motility J. Biol. Chem., January 28, 2005; 280(4): 3112 - 3120. [Abstract] [Full Text] [PDF] |
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