Free radical mediated photoreceptor damage in uveitis

Free radical mediated photoreceptor damage in uveitis 1 <h5>Introduction</h5> Uveitis and other intraocular inflammations are complex, acute or chronic inflammatory processes that primarily involve the uvea. The process can extend, however, to involve the retina, intraocular cavities, optic nerve and other ocular structures. Chronic intraocular inflammation is a major cause of blindness. This loss of vision is the result of damage inflicted by the inflammatory cell infiltration, particularly the release of various cytokines or other mediators, including oxygen metabolites ( Rao, 1990 ). The inflammatory cells that participate in chronic uveitis include lymphocytes, both T and B cells of various subtypes, and phagocytic cells, such as macrophages which derive from circulating monocytes. In addition, local tissue cellular components also participate, either by enhancing the inflammation or by down-regulating the process. In the uvea, these cellular components are vascular endothelia and melanocytes. In the retina, the cellular components that participate in the process include microglia, astrocytes, Müller cells, photoreceptors, and retinal pigment epithelium (RPE). The latter appears to play an active role in the modulation of uveitis and other intraocular inflammations including intraocular infections caused by various microbial agents, not only because of its anatomic location but because of its ability to generate either pro- or http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Progress in Retinal and Eye Research Elsevier

Free radical mediated photoreceptor damage in uveitis

Progress in Retinal and Eye Research, Volume 19 (1) – Jan 1, 2000

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Publisher
Elsevier
Copyright
Copyright © 1999 Elsevier Science Ltd
ISSN
1350-9462
eISSN
1873-1635
D.O.I.
10.1016/S1350-9462(99)00003-8
Publisher site
See Article on Publisher Site

Abstract

1 <h5>Introduction</h5> Uveitis and other intraocular inflammations are complex, acute or chronic inflammatory processes that primarily involve the uvea. The process can extend, however, to involve the retina, intraocular cavities, optic nerve and other ocular structures. Chronic intraocular inflammation is a major cause of blindness. This loss of vision is the result of damage inflicted by the inflammatory cell infiltration, particularly the release of various cytokines or other mediators, including oxygen metabolites ( Rao, 1990 ). The inflammatory cells that participate in chronic uveitis include lymphocytes, both T and B cells of various subtypes, and phagocytic cells, such as macrophages which derive from circulating monocytes. In addition, local tissue cellular components also participate, either by enhancing the inflammation or by down-regulating the process. In the uvea, these cellular components are vascular endothelia and melanocytes. In the retina, the cellular components that participate in the process include microglia, astrocytes, Müller cells, photoreceptors, and retinal pigment epithelium (RPE). The latter appears to play an active role in the modulation of uveitis and other intraocular inflammations including intraocular infections caused by various microbial agents, not only because of its anatomic location but because of its ability to generate either pro- or

Journal

Progress in Retinal and Eye ResearchElsevier

Published: Jan 1, 2000

References

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