Heat shock proteins, immunity and glaucoma

Brain Res Bull. 2004 Feb 15;62(6):473-80. doi: 10.1016/S0361-9230(03)00074-1.


Glaucoma is no longer viewed simply as elevated intraocular pressure (IOP) that damages the optic nerve. In addition to high IOP, evidence is rapidly accumulating that suggests damage to the optic nerve may be initiated or sustained by any number of factors including ischemia, excitotoxicity, neurotrophin insufficiency, peroxynitrite damage or others not yet defined. These different harmful influences then likely act through common final pathways that eventually activate the cellular proteases that accompany neuronal programmed cell death. We believe aberrant immune signal processing may also result in retinal ganglion cell death. We hypothesized that one form of glaucoma may be an autoimmune neuropathy in which an individual's immune system is not only inappropriately regulated, but a cytotoxic effect is rendered by the very system which normally serves to protect it against stress. We propose that the family of proteins termed "heat shock proteins" are critical modulators of both the homeostatic/cytoprotective as well as pathogenic/neurodegenerative arms of the immune system in retinal ganglion cells or glial cells and are thus integral to glaucomatous neurodegeneration.

Publication types

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

MeSH terms

  • Animals
  • Glaucoma / immunology*
  • Glaucoma / metabolism*
  • Heat-Shock Proteins / immunology*
  • Heat-Shock Proteins / metabolism*
  • Humans
  • Immunity / physiology


  • Heat-Shock Proteins