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Related Experiment Videos

Atherosclerosis--an autoimmune disease.

G Wick1, Q Xu

  • 1Institute for Biomedical Aging Research of the Austrian Academy of Sciences, Rennweg 10, 6020, Innsbruck, Austria. Georg.Wick@oeaw.ac.at

Experimental Gerontology
|May 19, 2000
PubMed
Summary

Immune responses to microbial heat shock protein 60 (HSP 60) may trigger atherosclerosis due to cross-reactivity with human HSP 60. This immunological hypothesis offers new diagnostic and therapeutic strategies for atherosclerosis.

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Area of Science:

  • Immunology
  • Cardiovascular Research
  • Pathogenesis

Background:

  • Immune-inflammatory processes are implicated in atherosclerosis development.
  • Atherosclerosis pathogenesis may involve immune reactions.
  • Heat shock protein 60 (HSP 60) is a key factor.

Purpose of the Study:

  • To present an "immunological" hypothesis of atherogenesis.
  • To explore the role of immune responses to microbial HSP 60 in atherosclerosis.
  • To investigate potential cross-reactivity between microbial and human HSP 60.

Main Methods:

  • Review of existing data on immune reactions to HSP 60.
  • Analysis of antigenic homology between microbial and human HSP 60.
  • Examination of endothelial cell responses to stress factors and HSP 60.

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Main Results:

  • Widespread protective immunity against microbial HSP 60 exists.
  • Significant antigenic homology between microbial and human HSP 60 is observed.
  • Endothelial cells in stressed arteries express human HSP 60 and adhesion molecules.

Conclusions:

  • Cross-reactivity with human HSP 60, due to immune responses to microbial HSP 60, may drive atherogenesis.
  • This immunological concept opens new diagnostic avenues for atherosclerosis.
  • The hypothesis provides a basis for novel therapeutic interventions in atherosclerosis.