title: Immunopathogenesis of atherosclerosis.
abstract: Recent clinical studies indicate that the number of microbial infections (the "pathogen burden") critically determines the development and progression of atherosclerotic disease. Viruses or bacteria with a specific tropism for cells of the vascular wall may contribute to the initial vascular injury via direct cytopathic effects or via the induction of genuine autoimmune responses. Immunopathological processes such as molecular mimicry, epitope spreading, or bystander activation of self-reactive lymphocytes most likely fuel the chronic inflammatory process in the vascular wall. Recognition of atherogenesis as a pathogen-driven, immunopathological process makes this disease amenable to new treatment strategies such as vaccination or immunomodulation.
authors.affiliation: Research Departmrnt, Kantonal Hospital St. Gallen, 9007 St. Gallen, Switzerland. Burkhard.Ludewig@kssg.ch
authors.forename: Burkhard
authors.initials: B
authors.lastname: Ludewig
authors.forename: Philippe
authors.initials: P
authors.lastname: Krebs
authors.forename: Elke
authors.initials: E
authors.lastname: Scandella
mesh_terms: D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology / Q000276:immunology* / Q000503:physiopathology; D002319:Cardiovascular System / Q000276:immunology* / Q000382:microbiology; D003141:Communicable Diseases / Q000150:complications / Q000276:immunology* / Q000503:physiopathology; D000939:Epitopes / Q000276:immunology; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology; D018716:Molecular Mimicry / Q000276:immunology
chemical_list: D000939:Epitopes