April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Origin and Antigen Presentation Function of Retinal Dendritic Cells
Author Affiliations & Notes
  • Scott W. McPherson
    Department of Ophthalmology, University of Minnesota, Minneapolis, Minnesota
  • Neal Heuss
    Department of Ophthalmology, University of Minnesota, Minneapolis, Minnesota
  • Ute Lehmann
    Department of Ophthalmology, University of Minnesota, Minneapolis, Minnesota
  • Dale S. Gregerson
    Department of Ophthalmology, University of Minnesota, Minneapolis, Minnesota
  • Footnotes
    Commercial Relationships  Scott W. McPherson, None; Neal Heuss, None; Ute Lehmann, None; Dale S. Gregerson, None
  • Footnotes
    Support  NIH Grants RO1-EY011542, RO1-EY016376, P30-EY011374, Research to Prevent Blindness, MInnesota Lions Club
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 2304. doi:https://doi.org/
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    • Get Citation

      Scott W. McPherson, Neal Heuss, Ute Lehmann, Dale S. Gregerson; Origin and Antigen Presentation Function of Retinal Dendritic Cells. Invest. Ophthalmol. Vis. Sci. 2011;52(14):2304. doi: https://doi.org/.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : Previously, we showed that the quiescent retina contains a small number of dendritic cells (DC) that are highly responsive to retinal injury. The purpose of this study is to determine the origin of these retinal DC and to determine if they possess the ability to present antigen typically associated with DC.

Methods: : CD11c-DTR mice, which expressed both green fluorescent protein (GFP) and diptheria toxin (Dtx) under control of the CD11c promoter, were used to visualize or deplete DC. Upregulation of retinal DC was done by optic nerve crush (ONC) injury. DC origin studies were done using radiation bone marrow chimeras (RBMC) between wild type and CD11c-DTR mice. Whole retinas were flat-mounted and examined by fluorescence microscopy. The ability of retinal DC to induce regulatory T cells (Tregs) or effector T cells was assayed using T cells from FoxP3DTR-BG2 mice (a CD4+ TCR transgenic specific for beta-galactosidase expressing GFP and Dtx on FoxP3+ cells).

Results: : RBMC studies combined with fluorescence microscopy showed that retinal DC could be derived from both local hematopoietic progenitor cells and from circulating CD45+ myeloid precursor cells. However, retinal injury was required for the efficient recruitment of cells from the circulation. Microglia isolated from quiescent and injured retinas could not be induced to express CD11c when cultured with INF-g and GM-CFS. DC (CD11c+) cells isolated from quiescent retinas had greater ability to induce Tregs, while DC from injured retinas induced T cell proliferation and activation compared to CD11c- cells or CD11c+ cells from quiescent retinas.

Conclusions: : These results support our earlier findings that the retina contains a population of DC that are distinct from microglia and are the cells that respond to retinal injury. Further, the ability to stimulate both Tregs and effector T cells suggests that retinal DC are likely involved in the immune responses associated with neuroprotection and neurodegeneration.

Keywords: antigen presentation/processing • immunomodulation/immunoregulation • immune tolerance/privilege 
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