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J. Hung, M. Evans, K.A. Tawansy, N.A. Rao; Immunohistochemical Analysis of Inflammatory Cells in Pediatric Epiretinal Membranes of Diverse Causes . Invest. Ophthalmol. Vis. Sci. 2006;47(13):5054.
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The development of epiretinal membranes may either be asymptomatic or cause visual distortion and can be seen in conditions that include intraocular inflammations, proliferative retinopathies, vitreous hemorrhages, and traumatic injuries. These epiretinal membranes show varying proportions of infiltrating inflammatory cells; however, it is not clear whether such inflammatory cells differ in their distribution and phenotypic expression of surface molecules in different ocular conditions.
We evaluated 15 epiretinal membranes that were surgically obtained during vitrectomies from pediatric eyes with clinical diagnoses of retinopathy of prematurity (6 cases), uveitis (4 cases), ocular toxocariasis (3 cases), or Norrie disease (2 cases). Histologic sections were prepared for staining with GFAP, CLA, CD3, CD20, CD34, CD68, and CD45. The stains were evaluated for distribution of glial cells, the presence of leucocytes, and neovascular channels.
Twelve (80%) of the 15 epiretinal membranes revealed GFAP–positive cells. CD34–positive vessels were noted in 12 of the 15 cases. Infiltration by macrophage cells, as shown by CD68–marker, was seen in 12 cases. CD45–positive cells were found in 14 cases. All 15 cases revealed CD3–positive cells, and their numbers were markedly increased in the cases with uveitis and ocular toxocariasis. None of the 6 cases of retinopathy of prematurity revealed CD20–positive cells, while 6 of the remaining 9 cases showed very few CD20–positive cells.
The inflammatory infiltrate made up of primarily T–cells is a prominent feature in intraocular inflammatory diseases such as uveitis and ocular toxocariasis. B–cells may be found in the membranes of eyes with uveitis and ocular toxocariasis, but they are absent in eyes with retinopathy of prematurity. This study suggests that macrophages play a role in the pathogenesis of epiretinal membrane formation, irrespective of the primary cause of retinal damage.
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