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N. Kawanaka, A. W. Taylor; Expression of Suppressor Macrophage Markers in the Immune Privileged Retina. Invest. Ophthalmol. Vis. Sci. 2007;48(13):5202.
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© ARVO (1962-2015); The Authors (2016-present)
Our previous work suggests that while retinal pigmented epithelial cells (RPE) suppress inflammatory activity in activated macrophages they promote activation of suppressor macrophages. The suppressor macrophages are characterized by the simultaneous expression of nitric oxide synthase 2 (NOS2) and Arginase 1. Therefore, we examined the retina for the presence of potential suppressor macrophages in healthy and wounded mouse retinas.
Paraffin fixed sections were made from C57BL/6J mouse eyes with healthy retinas, and from eyes with wounded retinas caused by OcuLight SLx Diode laser burns 3 days prior to collection. The sections were stained for macrophage makers using antibodies against CD11b or CD64, and with antibodies against the enzymes NOS2 or Arginase 1.
Macrophages in healthy retinas expressed both Arginase 1 and NOS2 together; however, the population of the cells in the retina was low. The stained cells were restricted to the inner nuclear layer of the retina. In contrast, macrophages in wounded retinas were found in the wound site, and in the ganglion cell layer and choroid around the wound site. The population of these cells was abundant. Also, there was an increase of macrophages that stained with NOS2 or Arginase1 only. Interestingly we found that beyond the wound site the staining pattern of macrophages was no different from the staining of healthy retinal tissues.
In the healthy retina there is a low number of macrophages, which all express the markers of suppressor macrophages. However, in the early stages of retinal wounding more macrophages with only inflammatory or wound repairing markers are observed around the wound site. These macrophages are probably recent migrants in response to the wounding. These results further demonstrate that ocular immune privilege promotes the activation of suppressor macrophages in the retina, and suggest that retinal wounding that brakes immune privilege will shift macrophage functionality to inflammation and wound repair.
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