Role of heat shock protein 65/60 in the pathogenesis of atherosclerosis

Int Arch Allergy Immunol. 1995 May-Jun;107(1-3):130-1. doi: 10.1159/000236952.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Arteriosclerosis / epidemiology
  • Arteriosclerosis / etiology*
  • Arteriosclerosis / immunology
  • Arteriosclerosis / pathology
  • Bacterial Proteins*
  • CD4-Positive T-Lymphocytes / immunology
  • CD4-Positive T-Lymphocytes / pathology
  • Cell Adhesion Molecules / analysis
  • Chaperonin 60 / immunology
  • Chaperonin 60 / physiology*
  • Chaperonins / immunology
  • Chaperonins / physiology*
  • Diet, Atherogenic
  • Humans
  • Intercellular Adhesion Molecule-1 / analysis
  • Rabbits
  • Risk Factors
  • Vascular Cell Adhesion Molecule-1

Substances

  • Bacterial Proteins
  • Cell Adhesion Molecules
  • Chaperonin 60
  • Vascular Cell Adhesion Molecule-1
  • heat-shock protein 65, Mycobacterium
  • Intercellular Adhesion Molecule-1
  • Chaperonins