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K.-H. Sonoda, T. Oshima, S. Nakao, T. Ishibashi; The Protective Role of CD1d-Reactive Invariant NKT Cells in Cauterization-Induced Acute Corneal Inflammation. Invest. Ophthalmol. Vis. Sci. 2007;48(13):192.
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© ARVO (1962-2015); The Authors (2016-present)
Natural Killer T (NKT) cells belong to a specialized population of lymphocytes that coexpress the T cell receptor and NK marker. CD1d-reactive NKT cells are required for induction of allospecific regulatory T cells and are essential for survival of corneal allografts. Although allospecific T cells mediated chronic corneal allograft rejection, acute corneal inflammation were induced by various stimuli (including chemical burn, trauma and etc.) and mainly mediated by neutrophils/macrophages. We thus examined the role of invariant NKT cells in a cauterization-induced acute corneal inflammation.
The corneas were cauterized with silver nitrate in control mice and two independent NKT cell-deficient mice; CD1d knockout (KO) mice and Ja18 KO mice. Clinical signs such as corneal edema and opacity were examined and the phenotypes of the cells infiltrating the cornea were analyzed by flow cytometry at 96 h after cauterization. We also examined the cytokine expression in cauterized cornea by RT-PCR.
After cauterization, both CD1d KO and Ja18 KO mice significantly increased the levels of corneal edema and opacity compared to control mice 96h later. Although the number of infiltrating cells was not significantly different at 96h, early neutrophil accumulation (24h) was significantly increased in both NKT cell-deficient mice. Importantly, early production of VEGF, IFNg, and TNFa in cauterized cornea was observed in both NKT cell-deficient mice, but not in control mice.
NKT cells might regulate early accumulation of neutrophils, protect cornea from excessive inflammation and maintain corneal clarity.
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