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 simpl ex 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 a nd HSV-1 immune CD4+ and CD8+ subsets from Igh-1 disparate BALB/c cong enic mice were adoptively transferred into athymic BALB/c nude mice, w hich 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 mic e resulted in the development of only a mild keratitis in 50% of the r ecipients. Transfer of CD8+ cells from either donor strain did not res ult in stromal disease in any recipient mouse. These results clearly d emonstrate the pivotal role of CD4+ T cells in the development of necr otizing herpes stromal keratitis, and further demonstrate that CD8+ T cells are not essential in HSK development in the BALB/c system.