Defects in regulation of local immune responses resulting in atherosclerosis.
Atherosclerosis is nowadays generally accepted as an inflammatory disease but the mechanism of its origin and development have not yet been fully clarified. The present review focuses on the role of the local immune system as one of the key players in the pathogenesis of the complex process. Its part represented by vascular-associated lymphoid tissue (VALT) within the arterial wall participates directly in the vascular wall's homeostatis. Its inordinate activation during ontogenic development of an individual, this formerly defensive and physiologic mechanism transform into a pathological process resulting in an impairing inflammation. Hsp60, CRP and oxidized or otherwise modified LDL are serious candidates for triggering these pathological changes. The principal role is played by anti-Hsp60 antibodies and by shear stress originating on the surface of endothelium due to blood flow. The experimental and clinical data supporting this immunological hypothesis of atherosclerosis are discussed.
Ferencík
Miroslav
M
Institute of Immunology, Faculty of Medicine, Comenius University, Bratislava, Slovak Repoublic. miroslav.ferencik@fmed.uniba.sk
Stvrtinová
Viera
V
Hulín
Ivan
I
D000818:Animals; D050197:Atherosclerosis / Q000209:etiology* / Q000276:immunology*; D015551:Autoimmunity; D002097:C-Reactive Protein / Q000276:immunology; D019013:CD40 Antigens / Q000276:immunology; D023201:CD40 Ligand / Q000276:immunology; D018834:Chaperonin 60 / Q000276:immunology; D004730:Endothelium, Vascular / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate; D018836:Inflammation Mediators / Q000276:immunology; D018448:Models, Immunological
D019013:CD40 Antigens; D018834:Chaperonin 60; D018836:Inflammation Mediators; D023201:CD40 Ligand; D002097:C-Reactive Protein