Abstract

IFN-γ acts to promote the severity of experimental allergic conjunctivitis (EC) during the effector phase. To identify the cell source and cell target of this cytokine in the effector phase of EC, we established mice lacking both IFN-γ and the IFN-γ receptor (Dbl-KO). Reciprocal adoptive transfer experiments involving wild-type, Dbl-KO, IFN-γ-lacking and IFN-γR-lacking mice were performed. EC was then induced by RW challenge in eye drops. Analysis of the resulting eosinophil infiltration in the six donor/recipient combinations revealed that IFN-γ produced by both donor and recipient cells plays an important role in the EC effector phase, and that the targets for this cytokine are also both donor and recipient cells. That EC was attenuated when any of the IFN-γ-IFN-γR interactions were disturbed confirms that IFN-γ promotes the severity of EC during the effector phase. These observations indicate that Dbl-KO mice will be useful for investigating the role(s) IFN-γ play in inflammatory diseases.

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