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Yuan Gao, Zhijie Li, Clifton W. Smith; ICAM-1 is Necessary for Efficient Accumulation of CD11c+ Cells in Healing Corneal Epithelium. Invest. Ophthalmol. Vis. Sci. 2012;53(14):6180.
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© ARVO (1962-2015); The Authors (2016-present)
The current work is to define the contribution of Intercellular Adhesion Molecule-1 (ICAM-1) to the trafficking of CD11c positive cells after corneal abrasion.
The central corneal epithelial abrasion (2 mm) was performed in the female C57BL/6 mice. Corneas were collected at 12, 24, 36, 48, 60, 72 and 96 hrs after injury. The dynamic response of central and peripheral CD11c+ cells in murine cornea to various time points after injury were examined and analyzed by using fluorescence deconvolution microscopy. Epithelium was analyzed by qrtPCR and immunocytology at various time points after central epithelial abrasion in female wild-type and ICAM-1-/- C57BL/6 mice. These ICAM-1-/- mice have a null mutation without expression of alternative forms of ICAM-1.
Wounded wild-type epithelium significantly expressed ICAM-1, and MCP-1, known to attract myeloid cells, was markedly elevated within the first 24 hours. In the normal limbus, some CD11c+ cells with and without dendritic morphology were found in the epithelium and corneal stroma. After wounding, many CD11c+ cells accumulated in the epithelium. These cells were predominantly without dendritic morphology, and they extended from limbal to central cornea, peaking at 48 hours. Wild-type mice had an approximate fourfold increase in epithelial CD11c+ cells at 48 hours after epithelial abrasion, while ICAM-1-/- mice had 36.0% (p<0.01) fewer CD11c+ cells. 1.8% of the CD11c+ cells migrated into the center of the cornea at 48 hrs after epithelial abrasion, while no CD11c+ cells were observed in the central corneas of ICAM-1-/- mice. The accumulation and distribution of CD11c+ cells were significantly depressed by using anti-ICAM-1 blocking antibody in wild-type mice, and epithelial healing was significantly delayed.
ICAM-1 expression in corneal epithelium appears to be actively involved in the trafficking of CD11c+ cells.
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