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Chronic Infections and Atherosclerosis
Author(s) -
AYADA KIYOSHI,
YOKOTA KENJI,
KOBAYASHI KAZUKO,
SHOENFELD YEHUDA,
MATSUURA EIJI,
OGUMA KEIJI
Publication year - 2007
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1422.062
Subject(s) - immunology , heat shock protein , immune system , autoimmunity , molecular mimicry , hsp60 , antibody , medicine , inflammation , disease , coronary artery disease , biology , pathology , hsp70 , biochemistry , gene
: Immunoinflammatory processes due to chronic infection are thought to be one of the definitive atherogenetic processes. Especially, anti‐heat shock protein antibodies have been related to the prevalence of disease such as coronary artery disease or cerebral infarction, etc., resulted from atherosclerosis. Furthermore, the presence of HSP60‐specific T lymphocytes in circulation may increase the risk of atherosclerosis. We have recently demonstrated the evidences that Helicobacter pylori infection induced atherosclerosis in apoe +/− ldlr +/− mice and that Hp ‐anti‐heat‐shock protein specific Th1‐dominant immune responses had a major involvement in the progression of atherosclerosis. These cellular immune responses caused autoimmunity against endogenous HSP60 (expressed on the stressed cells of vascular endothelium), due to the molecular mimicry. Therefore, an appropriate treatment with antibiotics or with anti‐HSP60 antibodies, which regulates the Th1 induction, could sufficiently reduce the progression of atherosclerosis .