Study of cellular immune responses against herpetic keratitis

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We first analyzed major histocompatibility (MHC) antigen expressionand infiltrated cell populations in HSV-infected murine corneas. By immunohistochemistry, stromal keratocytes have been shown to begin to express class II MHC antigens following herpetic infection in the cornea, along with numerous T lymphocytes mediating delayed type hypersensitivity (DTH) reactions. Thus, effective suppression of these inflammatory cells may lead to minimal corneal scarring. In the next study, anterior chamber-associated immune deviation (ACAID) which has been shown to suppress DTH was investigated as a new therapeutic modality against stromal herpes. The mice that had received intracameral injection of HSV-antigens developed much less stromal opacity as compared with controls. This effect was also confirmed by cell transfer experiments using athymic nude mice.Another way to control corneal herpes is to inhibit the establishment of ganglionic latency. A truncated-glycoprotein D (_9D)-interleukin-2 (IL-2),which is capable of inducing cellular immunity unlike other subunit vaccine candidates, suppressed the development of epithelial as well as stromal lesions but could not inhibit the trigeminal ganglionic latency. The dosis or timing for administration should be reconsidered.In another study, a variety of inbred mice were topically inoculated with HSV without scarification. Each inbred mouse strain was shown to exhibit different susceptibility to topical HSV challenge. Non-specific, local defense mechanisms may be operative for this phenomenon.