Immune mechanisms in atherosclerosis.
Atherosclerosis is an inflammatory disease. Its lesions are filled with immune cells that can orchestrate and effect inflammatory responses. In fact, the first lesions of atherosclerosis consist of macrophages and T cells. Unstable plaques are particularly rich in activated immune cells, suggesting that they may initiate plaque activation. We have seen a rapid increase in the understanding of the mechanisms that govern the recruitment, differentiation, and activation of immune cells in atherosclerosis. Experimental research has identified several candidate antigens, and there are encouraging data suggesting that immune modulation as well as immunization can reduce the progression of the disease. This review provides an overview of our current understanding of the role of immune mechanisms in atherosclerosis.
Hansson
G K
GK
Center for Molecular Medicine and the Department of Medicine at Karolinska Hospital, Karolinska Institute, Stockholm, Sweden. Goran.Hansson@cmm.ki.se
D000276:Adjuvants, Immunologic / Q000627:therapeutic use; D000818:Animals; D001161:Arteriosclerosis / Q000276:immunology* / Q000517:prevention & control; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D015815:Cell Adhesion Molecules / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D006360:Heat-Shock Proteins / Q000276:immunology; D006801:Humans; D007111:Immunity, Cellular / Q000276:immunology; D007114:Immunization / Q000379:methods; D018799:Intercellular Adhesion Molecule-1 / Q000276:immunology; D020556:Neutrophil Infiltration / Q000276:immunology
D000276:Adjuvants, Immunologic; D015815:Cell Adhesion Molecules; D016207:Cytokines; D006360:Heat-Shock Proteins; D018799:Intercellular Adhesion Molecule-1