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Heat Shock Proteins in Rheumatoid Arthritis

  • W. van Eden
Part of the Handbook of Experimental Pharmacology book series (HEP, volume 136)

Abstract

In view of the fundamental role of stress proteins in the maintenance of protein homeostasis, it seems likely that malfunctions associated with members of stress protein families would have pathological effects. Such effects might be minimal under normal physiological conditions, but could be exacerbated at times when other disease stimuli trigger the requirement for local alterations in stress protein function in particular afflicted cells or tissues. During infection, it can be anticipated that the requirement of stress proteins for cell viability will be equally essential both for the pathogen and for the infected host. Just as stress proteins are essential in “normal” as well as stressed cells, it is clear that changes in stress protein expression will be associated with physiologically normal events accompanying infection as well as with any subsequent pathological events. In addition to the direct role of stress proteins in cell physiology, their potential medical influence is compounded by their ability to act as potent immunogens. Responses to microbial stress proteins are a prominent feature of the immune repertoire in patients and in experimental animals, and there has been wide discussion of the possibility that recognition of conserved, self-like, epitopes on such antigens could influence infectious and other diseases. Three broad hypotheses have been put forward concerning the relevance of immunological reactivity to stress proteins:

Keywords

Rheumatoid Arthritis Heat Shock Protein Stress Protein Adjuvant Arthritis Reactive Arthritis 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer-Verlag Berlin Heidelberg 1999

Authors and Affiliations

  • W. van Eden

There are no affiliations available

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