Is atherosclerosis an immunologically mediated disease?

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Abstract

In contrast to general beliefs, recent data from different laboratories have provided evidence that the first stages of atherosclerosis are of an inflammatory nature. Here, Georg Wick and colleagues suggest that an autoimmune reaction against heat shock protein 60 (Hsp60), expressed by endothelial cells in areas that are subject to increased haemodynamic stress, is the initiating event in atherogenesis. Humoral and T-cell-mediated immune responses against Hsp60 have both been demonstrated early in disease. This inflammatory stage, which is reversible and has even been found in children, may progress into fully developed and atherosclerotic lesions, displaying all the classical pathohistological and functional consequences, if additional risk factors such as high blood cholesterol levels, smoking and obesity, are present.

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  • Cited by (381)

    • Heat shock proteins and cardiovascular disease

      2014, Advances in Clinical Chemistry
      Citation Excerpt :

      Both HSPs and anti-HSPs have been shown to stimulate the production of proinflammatory cytokines [48]. Wick and colleagues [124] have hypothesized that an immune response to HSPs, either endogenously derived from cells involved in atherogenesis or exogenously from microorganisms, may lead to complement-mediated endothelial injury and subsequent atherosclerosis. Mayr et al. reported that serum anti-HSP directed against Escherichia coli and C. pneumoniae-mediated lysis of stressed, but not unstressed endothelial cells [126].

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    This work was supported by the Austrian Research Council (Project No. 8925/MED.), the Austrian Ministry of Science and Research, and the Sandoz Foundation for Gerontological Research. We would like to thank Anya Mair for competent technical help, G. Jürgens and R. Kofler for fruitful discussions, as well as all collaborators for their cooperation on this project. We also thank Margit Kirchebner for secretarial help and Ilona Atzinger for preparing the figures.

    1

    Georg Wick, Georg Schett, Albert Amberger, Roman Kleindienst and Qingbo Xu are at the Institute for Biomedical Aging Research of the Austrian Academy of Sciences, Rennweg 10, A-6020 Innsbruck, Austria.

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