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Protective and Pathological Roles of Virus-Specific and Bystander CD8⁺ T Cells in Herpetic Stromal Keratitis¹

Kaustuv Banerjee^*, Partha Sarathi Biswas^*, Udayasankar Kumaraguru^*, Stephen P. Schoenberger and Barry T. Rouse^2,*

^* Comparative and Experimental Medicine, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996; and Division of Immune Regulation, La Jolla Institute of Allergy and Immunology, San Diego, CA 92121

Herpetic stromal keratitis (HSK), resulting from corneal HSV-1 infection, represents a T cell-mediated immunopathologic lesion. In T cell transgenic mice on a SCID or RAG knockout background, the T cells mediating lesions are unreactive to viral Ags. In these bystander models, animals develop ocular lesions but are unable to control infection. Transfer of HSV-immune cells into a CD8⁺ T cell bystander model resulted in clearance of virus from eyes, animals survived, and lesions developed to greater severity. However, the adoptively transferred CD8⁺ T cells were not evident in lesions, although they were readily detectable in the lymphoid tissues as well as in the peripheral and CNS. Our results indicate that viral-induced tissue damage can be caused by bystander cells, but these fail to control infection. Immune CD8⁺ T cells trigger clearance of virus from the eye, but this appears to result by the T cells acting at sites distal to the cornea. A case is made that CD8⁺ T cell control is expressed in the trigeminal ganglion, serving to curtail a source of virus to the cornea.

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