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C. W. Smith, S. Byeseda, A. Burns, Z. Li; CD11d, Epithelial ICAM-1 and T Cells in the Mouse Cornea. Invest. Ophthalmol. Vis. Sci. 2008;49(13):434.
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Following central corneal epithelial abrasion, murine γΔ T cells increase in the limbal and paralimbal epithelium, peaking at 18 to 24 hours after injury. This increase is reduced significantly in ICAM-1 deficient mice, but not in CD11a (LFA-1, αLβ2) deficient mice. In the current study, we investigated potential mechanisms involved in the increase of γΔ T cells that follows central corneal abrasion.
Central corneal epithelial abrasion (2 mm diameter) without stromal injury was performed in wildtype (C57BL/6J), Itgam-/- (CD11b deficient), Itgad-/- (CD11d deficient) or Icam1-/- mice. At various times following abrasion limbal and paralimbal epithelium was analyzed by rtPCR or immunofluorescence.
Regarding CD18 (β2) family adhesion molecules, CD11b deficiency failed to prevent γΔ T cell increases, but CD11d-deficient mice exhibited >60% reduction (p<0.01) in γΔ T cells at 18 and 24 hours after abrasion. ICAM-1 a potential ligand for CD18 (β2) integrins was upregulated (mRNA by 26 fold) and limbal and paralimbal epithelium bound anti-ICAM-1 within 3 hours after injury. Increases in γΔ T cells at 3 hours occurred within wildtype epithelium expressing ICAM-1, but not in ICAM-1-deficient mice. Real time PCR analysis for chemokine receptors reported to be expressed by γΔ T cells revealed expression of CCR2, CCR3, CCR5, CCR9 and CCR10 at 3 hours as well as mRNA for chemokines recognized by each of these receptors.
CD11d/CD18 and epithelial ICAM-1 appear to be necessary for increases in γΔ T cells within peripheral murine corneal epithelium following central abrasion.
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