The immune response against heat shock protein 60 (HSP60) derived from pathogens causing chronic infections is thought to be an important pro-atherogenic mechanism because high serum levels of antibodies against HSP60 have been associated with atherosclerotic diseases, such as coronary artery diseases, or cerebro-vascular events. Furthermore, the presence of HSP60-specific T lymphocytes in circulation may increase the risk of atherosclerosis. Our recent in vitro and in vivo studies have also shown an association of Helicobacter pylori-HSP60 (Hp-HSP60) specific Th1 immune responses elicited by H. pylori infection with the progression of atherosclerosis in a hyperlipidemic mouse model. These Th1 dominant immune responses may cross-react with endogenous HSP60 expressed on stressed cells of the vascular endothelium, likely due to molecular mimicry. However, the exact mechanisms by which endothelial cells display their HSP60 molecule or present HSP60 antigenic epitopes on the surface are still unclear.

Original languageEnglish
Pages (from-to)44-48
Number of pages5
JournalClinical Reviews in Allergy and Immunology
Issue number1
Publication statusPublished - 2009


  • Atherosclerosis
  • Heat shock protein 60
  • Helicobacter pylori

ASJC Scopus subject areas

  • Immunology and Allergy


Dive into the research topics of 'Chronic infections and atherosclerosis'. Together they form a unique fingerprint.

Cite this