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Babak Baban, Folami Lamoke, Diana Gutsaeva, Manuela Bartoli; Dendritic cells-mediated polarization of retinal macrophages in human diabetic retina. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):4291.
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Systemic and tissue-specific inflammatory responses have been implicated in the pathogenesis of diabetic retinopathy (DR). There is a paucity of studies, however, on the identification of cellular components within the immune system that more directly are involved in hyperglycemia-induced retinal inflammatory responses. Few previous studies have suggested that in the diabetic retina there is an increase in inflammatory (M1) macrophages. In this study we wanted further analyzed the role of dendritic cells (DC) in promoting M2 (regulatory) to M1(inflammatory) macrophage skewing in human diabetic retina.
Eye globes of diabetic and not diabetic donors were purchased from Georgia Eye Bank. Immunohistochemical analysis was performed to identify myeloid (mDC, inflammatory) and plasmacytoid (pDC, tolerogenic) dendritc cells in human diabetic retinas as compared to not diabetic control retinas. Specific phenotypic markers were used to identify pDC (CD11c and B220) and M2 macrophages (CD68 and CD206) in the retinal tissue.
In human diabetic retina there was a decrease in immunoreactivity to phenotypic markers of M2 (double positivity to CD68 and CD206) regulatory macrophages in favor of M1 inflammatory macrophages (CD68 positive). This effect was correlated with decreased immunoreactivity for pDC markers and augmented mDC markers.
The obtained results are the first to determine that there is a migration and enrichment of myloid dendritic cells in the human diabetic retina and this correlate with M2 to M1 macrophage transition. These data reveal a potential key role for dendritic cells in DR pathogenesis
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