Identification of Novel Dendritic Cell Populations in Normal Mouse Retina

Abstract

A novel population of 33D1(+) DCs was identified in normal mouse retina. The function of these cells remains to be defined, but increased numbers correlate positively with structural abnormalities in the RPE and increased resistance of the strain to EAU.

Characterization of a Mouse Model of Hyperglycemia and Retinal Neovascularization

“…The peri-venular, but not peri-arteriolar, localization of MHC class II ϩ cells in a context of experimental autoimmune uveitis-induced blood retinal barrier breakdown was recently pointed out by Xu et al 50 Similar MHC class II ϩ distribution in VEGF-related pathology suggests that peri-venular pattern of staining is not specific to the mechanism of injury, but is yet another marker of the blood-tissue barrier breakdown in mice. Finally, without functional studies, the retinal MHC class II patterning in Kimba and Akimba does not allow for further deductions about (1) the actual success of antigen presentation or (2) involvement of retinal autoimmunity in these models.…”

“…39 The induction of MHC class II antigen expression is a common feature of various central nervous system pathologies, 48 where blood-tissue barrier is acutely or chronically compromised. In the retina, the MHC II antigen appears to rise with the blood-retina barrier dysfunction secondary to (1) ageing, 49 (2) range of pathologies, 49,50 and (3) possible strain-specific variations in the integrity of retinal pigment epithelium (in mice). 50 The findings of our study indeed conform to these notions: the hVEGF-mediated disruption of retinal vasculature as well as the RPE layer (Kimba and Akimba) drives abundant MHC class II ϩ up-regulation, in this case demonstrable with dendriform and round MHC class II ϩ cells surrounding the venules and saturating the juxtapapillary region and peripheral retina.…”

“…In the retina, the MHC II antigen appears to rise with the blood-retina barrier dysfunction secondary to (1) ageing, 49 (2) range of pathologies, 49,50 and (3) possible strain-specific variations in the integrity of retinal pigment epithelium (in mice). 50 The findings of our study indeed conform to these notions: the hVEGF-mediated disruption of retinal vasculature as well as the RPE layer (Kimba and Akimba) drives abundant MHC class II ϩ up-regulation, in this case demonstrable with dendriform and round MHC class II ϩ cells surrounding the venules and saturating the juxtapapillary region and peripheral retina. This is contrary to what is seen in C57Bl/6 and Akita mice, in which the morphological evidence of endothelial or RPE damage is absent.…”

Privilege revisited: an evaluation of the eye's defence mechanisms

“…In fact, experiments in which activated T cells have been intravenously administered to mice developing uveitis show that these cells reside at the initial site of contact between the T cell and the antigen-presenting cell. 53 Perhaps in the normal physiological state these peripheral antigen-presenting cells promote tolerance ('privilege') rather than immunity. It is interesting to note that many types of chronic posterior uveitis begin with lesions around the optic nerve or in the region of the pars plana/retinal periphery.…”

CD4 T-Cell Suppression by Cells fromToxoplasma gondii-Infected Retinas Is Mediated by Surface Protein PD-L1

“…This is because retinal MHC class II expression is low as a result of the high expression of immunosuppressive cytokines and the blood-ocular barrier (49). Regardless, retinal microglia, endothelial cells, retinal pigment epithelial (RPE) cells, and other, less well characterized cells can express MHC class II under certain conditions (18,25,57). But the identity and function of MHC class IIexpressing cells in Toxoplasma-infected retinas remain unknown.…”