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Debra A. Carter, Andrew D. Dick; CD133+ Retinal Progenitor Cell Function are Maintained by IL-27 Mediated IL-10 Expressing CD11b+ Microglia. Invest. Ophthalmol. Vis. Sci. 2011;52(14):3173.
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To promote healing and cell replacement following injury, inflammation or degeneration, retinal homeostasis needs to be redressed, in which microglia are known to play a significant role. Following identification and then purifying a population of CD133+ cells we have demonstrated that the adult human retina possess cells that despite limited proliferative capacity, remain candidates for cell renewal. Our present aim is to interrogate interaction of CD133+ progenitor cells and CD11b+ microglia, and gain understanding of the interaction between these two cell types. We aim to determine under which conditions cell replacement and neuronal/photoreceptor survival is promoted or inhibited.
Retinal cell suspensions were derived from adult human post-mortem tissue with ethical approval. CD133+ cells and CD11b+ cells were isolated using Automated Magnetic Cell (MACS®) sorting. We analysed gene expression, cytokine release and phenotype following co-culture of two cell types when exposed to LPS/IFNγ Purified CD133+ retinal cells and CD11b+ microglia gene expression was analysed via qPCR, for cell phenotype via flow cytometry and for cytokine release using both qPCR and BD cytokine arrays. Statistical analysis was performed using ANOVA (prism)
When CD133+ progenitor cells are co cultured with CD11b+ microglia, the relative expression of IL27 in CD133+ is increased significantly. Contemporaneously CD11b+ microglia increase their relative expression of IL10. In support, the relative expression of both IRF (STAT1) and SOCS3 (STAT3) were upregulated in both CD133+ progenitor cells and CD11b+ microglia. Following LPS activation the expression of both IL10 and IL27R increased in microglia.
The data supports a mutual interaction between the adult retinal progenitor niche of CD133+ cells and CD11b+-myeloid cell (microglia). These cells sustain an immunosuppressive environment via IL-27 medaited anti-inflammatory Il-10 production whilst maintaining the turnover of CD133+ cells.
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