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Review
. 2011 Aug;93(2):178-86.
doi: 10.1016/j.exer.2010.07.009. Epub 2010 Aug 13.

The immune response in glaucoma: a perspective on the roles of oxidative stress

Gülgün Tezel  1
Affiliations
Review

The immune response in glaucoma: a perspective on the roles of oxidative stress

Gülgün Tezel. Exp Eye Res. 2011 Aug.

Abstract

Neurodegenerative insults and glial activation during glaucomatous neurodegeneration initiate an immune response to restore tissue homeostasis and facilitate tissue cleaning and healing. However, increasing risk factors over a chronic and cumulative period may lead to a failure in the regulation of innate and adaptive immune response pathways and represent a route for conversion of the beneficial immunity into a neuroinflammatory degenerative process contributing to disease progression. Oxidative stress developing through the pathogenic cellular processes of glaucoma, along with the aging-related component of oxidative stress, likely plays a critical role in shifting the physiological equilibrium. This review aims to provide a perspective on the complex interplay of cellular events during glaucomatous neurodegeneration by proposing a unifying scheme that integrates oxidative stress-related risk factors with the altered regulation of immune response in glaucoma.

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Figures

Figure 1
Figure 1
Elevated intraocular pressure(IOP)-related factors play an important role in initiation and progression of glaucomatous neurodegeneration. The immune system responds to glaucomatous tissue stress and injury as an intrinsic effort to facilitate tissue cleaning and healing. However, if there is a failure in the regulation of immune response due to accumulation of risk factors, the protective immunity may turn into a neurodegenerative process contributing to disease progression.
Figure 2
Figure 2
Elevated intraocular pressure(IOP)-related factors can initiate neurodegenerative injury in glaucoma, but also trigger various cellular events. A complex interplay of these events, which exhibits important links to oxidative stress, may amplify the primary injury process and contribute to the progression of neurodegeneration. IOP-dependent versus IOP-independent components of the neurodegenerative injury is determined by individual susceptibility factors yet to be fully identified.
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References

    1. Agapova OA, Ricard CS, Salvador-Silva M, Hernandez MR. Expression of matrix metalloproteinases and tissue inhibitors of metalloproteinases in human optic nerve head astrocytes. Glia. 2001;33:205–216. - PubMed
    1. Agrawal A, Tay J, Yang GE, Agrawal S, Gupta S. Age-associated epigenetic modifications in human DNA increase its immunogenicity. Aging. 2010;2:93–100. - PMC - PubMed
    1. Ahmed F, Brown KM, Stephan DA, Morrison JC, Johnson EC, Tomarev SI. Microarray analysis of changes in mRNA levels in the rat retina after experimental elevation of intraocular pressure. Invest Ophthalmol Vis Sci. 2004;45:1247–1258. - PubMed
    1. Banks WA, Erickson MA. The blood-brain barrier and immune function and dysfunction. Neurobiol Dis. 2010;37:26–32. - PubMed
    1. Bauer J, Bradl M, Hickley WF, Forss-Petter S, Breitschopf H, Linington C, Wekerle H, Lassmann H. T-cell apoptosis in inflammatory brain lesions: destruction of T cells does not depend on antigen recognition. Am J Pathol. 1998;153:715–724. - PMC - PubMed

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