Innate and adaptive immunity in the pathogenesis of atherosclerosis.
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.
Center for Molecular Medicine and Department of Medicine, Karolinska Institute, Stockholm, Sweden. Goran.Hansson@ cmm.ki.se
Göran K
GK
Hansson
Peter
P
Libby
Uwe
U
Schönbeck
Zhong-Qun
ZQ
Yan
D000818:Animals; D000918:Antibody Specificity / Q000276:immunology; D001161:Arteriosclerosis / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology*; D001808:Blood Vessels / Q000276:immunology / Q000503:physiopathology; D016207:Cytokines / Q000276:immunology; D018450:Disease Progression; D006801:Humans; D007110:Immunity, Active; D007113:Immunity, Innate; D018836:Inflammation Mediators / Q000276:immunology; D008214:Lymphocytes / Q000276:immunology; D008264:Macrophages / Q000276:immunology
D016207:Cytokines; D018836:Inflammation Mediators