Immunopathogenic Mechanisms in Intraocular Inflammation

Forrester, John V.; McMenamin, Paul G.

doi:10.1159/000058745

Cited by 55 publications

(37 citation statements)

References 107 publications

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“…It is unknown how that occurs but a classical view from in vitro studies suggests it is unlikely to be an aggregated response to all of the stimuli to which they are exposed, 1 and recent data provides evidence that a number of pro-and anti-inflammatory cytokines commit macrophages to develop sets of nonoverlapping and mutually exclusive properties or programs. 8,25,26 Programming is determined by the first cytokine to which macrophages are exposed and an essential component of the program is the development of unresponsiveness to other activating cytokines.…”

Section: Discussionmentioning

confidence: 99%

Constitutive Retinal CD200 Expression Regulates Resident Microglia and Activation State of Inflammatory Cells during Experimental Autoimmune Uveoretinitis

Broderick

Hoek

Forrester

et al. 2002

The American Journal of Pathology

196

151

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Section: Discussionmentioning

confidence: 99%

Constitutive Retinal CD200 Expression Regulates Resident Microglia and Activation State of Inflammatory Cells during Experimental Autoimmune Uveoretinitis

Broderick

Hoek

Forrester

et al. 2002

The American Journal of Pathology

196

151

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“…In many of these, inflammation is thought to be initiated by eye-reactive T cells (26,28). In this study, we have dissected the pathogenesis of T cell-induced ocular inflammation by examining the complement of transcripts of major cytokines, chemokines, and chemokine receptors expressed in each of three animal models.…”

Section: Discussionmentioning

confidence: 99%

Inflammatory Mediators in Uveitis: Differential Induction of Cytokines and Chemokines in Th1- Versus Th2-Mediated Ocular Inflammation

Foxman

Zhang

Hurst³

et al. 2002

The Journal of Immunology

137

116

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Ocular inflammation leads to vision loss through the destruction and scarring of delicate tissues along the visual axis. To identify inflammatory mediators involved in this process, we used real time RT-PCR to quantify the expression of mRNA transcripts of 34 cytokines, 26 chemokines, and 14 chemokine receptors at certain time points during T cell-mediated ocular inflammation. We induced disease by adoptive transfer of Ag-specific Th1 or Th2 cells into recipients expressing the target Ag in their eyes. We also compared the mediator expression patterns seen in adoptive transfer-induced inflammation with that seen in mouse eyes developing experimental autoimmune uveoretinitis. In addition, we used laser capture microdissection to examine chemokine mRNA production by both retinal pigment epithelium cells and infiltrating leukocytes in inflamed eyes. Major findings included the following: 1) Three patterns of expression of the inflammation-related molecules were seen in recipients of adoptively transferred Th cells: preferential expression in Th1 recipients, or in Th2 recipients, or similar expression in both recipient groups. 2) In experimental autoimmune uveoretinitis, the inflammatory mediator expression pattern largely paralleled that seen in Th1-induced disease. 3) Both retinal pigment epithelium and infiltrating leukocytes expressed chemokine transcripts in distinct, but overlapping patterns in inflamed eyes. 4) Interestingly, trancripts of multiple cytokines, chemokines, and chemokine receptors were constitutively expressed in high levels in mouse eyes. Seven of these molecules have not been previously associated with the eye. These data underscore the multiplicity of mediators that participate in the pathogenesis of eye inflammation and point to upstream cytokines as potential therapeutic targets.

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“…Associations have been reported between the breakdown of the blood retinal barrier and almost every retinal disease, particularly vascular retinopathies and pigment epitheliopathies (Forrester and Menamin, 1999). Inflammation-mediated damage to the neurosensory retina and RPE may affect the basic photochemical process of vision.…”

Section: Blood Retinal Barrier Permeabilitymentioning

confidence: 99%

Bacterial endophthalmitis: Therapeutic challenges and host–pathogen interactions

Callegan

Gilmore

Gregory

et al. 2007

Progress in Retinal and Eye Research

156

153

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Endophthalmitis is an infection of the posterior segment of the eye that frequently results in loss of vision. This devastating result occurs despite prompt and often aggressive therapeutic and surgical intervention. Over the past decade, research has centered on determining the bacterial and host factors involved in this potentially blinding disease. The initial focus on the bacterial factors responsible for intraocular virulence has recently expanded into analysis the inflammatory response to infection, including the molecular and cellular interactions between the pathogen and host. This review discusses the epidemiology and therapeutic challenges posed by endophthalmitis, as well as recent findings from the analysis of interactions between the host and pathogen. Based on these findings, a model for the pathogenesis of endophthalmitis is presented. A more comprehensive understanding of the molecular and cellular interactions taking place between pathogen and host during endophthalmitis will expose possible therapeutic targets designed to arrest the infection and prevent vision loss.

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Immunopathogenic Mechanisms in Intraocular Inflammation

Cited by 55 publications

References 107 publications

Constitutive Retinal CD200 Expression Regulates Resident Microglia and Activation State of Inflammatory Cells during Experimental Autoimmune Uveoretinitis

Constitutive Retinal CD200 Expression Regulates Resident Microglia and Activation State of Inflammatory Cells during Experimental Autoimmune Uveoretinitis

Inflammatory Mediators in Uveitis: Differential Induction of Cytokines and Chemokines in Th1- Versus Th2-Mediated Ocular Inflammation

Bacterial endophthalmitis: Therapeutic challenges and host–pathogen interactions

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