Role of heat shock protein 65/60 in the pathogenesis of atherosclerosis.
Investigations in rabbits and humans have provided experimental evidence that autoimmune reactions play a major role in the initial stages of the development of atherosclerosis. These involve the infiltration of the arterial intima with T cells reacting with heat shock protein (hsp) 65/60 and the occurrence of anti-hsp 65/60 antibodies. This early immunologically mediated stage of atherosclerosis is still reversible but if additional risk factors, such as high cholesterol levels, come into effect, severe mostly irreversible lesions develop.
Wick
G
G
Institute for Biomedical Aging Research, Austrian Academy of Sciences, Innsbruck.
Kleindienst
R
R
Schett
G
G
Amberger
A
A
Xu
Q
Q
D000818:Animals; D001161:Arteriosclerosis / Q000453:epidemiology / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D001426:Bacterial Proteins; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000473:pathology; D015815:Cell Adhesion Molecules / Q000032:analysis; D018834:Chaperonin 60 / Q000276:immunology / Q000502:physiology*; D018833:Chaperonins / Q000276:immunology / Q000502:physiology*; D004036:Diet, Atherogenic; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D011817:Rabbits; D012307:Risk Factors; D019010:Vascular Cell Adhesion Molecule-1
D001426:Bacterial Proteins; D015815:Cell Adhesion Molecules; D018834:Chaperonin 60; D019010:Vascular Cell Adhesion Molecule-1; C074119:heat-shock protein 65, Mycobacterium; D018799:Intercellular Adhesion Molecule-1; D018833:Chaperonins