THE ROLE OF IGH-1 DISPARATE CONGENIC MOUSE T-LYMPHOCYTES IN THE PATHOGENESIS OF HERPETIC STROMAL KERATITIS

The corneal destruction associated with herpes simplex keratitis (HSK) is primarily the result of the host's immune response to herpes simplex virus type-1 (HSV-1) infection. We examined the role of T cells and T cell subsets in the pathogenesis of HSK. Naive and immune T cells and HSV-1 immune CD4+ and CD8+ subsets from Igh-1 disparate BALB/c congenic mice were adoptively transferred into athymic BALB/c nude mice, which normally do not develop HSK. The results demonstrated that while the transfer of naive T cells from either HSK-susceptible C.AL-20 (Igh-1(d)) or HSK-resistant C.B-17 (Igh-l(b)) mice had little influence on HSK development, transfer of either CD3+ or CD4+ HSV-1 immune T cells from C.AL-20 mice resulted in the development of severe HSK in all of the recipients. Transfer of the same cell populations from C.B-17 mice resulted in the development of only a mild keratitis in 50% of the recipients. Transfer of CD8+ cells from either donor strain did not result in stromal disease in any recipient mouse. These results clearly demonstrate the pivotal role of CD4+ T cells in the development of necrotizing herpes stromal keratitis, and further demonstrate that CD8+ T cells are not essential in HSK development in the BALB/c system.