作者: Robert L. Hendricks , Randy J. Epstein , Terrence Tumpey
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摘要: Previous studies have revealed that herpes simplex virus type 1 (HSV-1) corneal stromal lesions do not develop in the absence of a cell-mediated immune (CMI) response to HSV-1 antigens. glycoprotein C (gC) has been shown play an important role induction cytotoxic T lymphocyte (CTL) infections at anatomical sites other than eye. Here we report deletion mutant lacking gC (gC-39) when used infect corneas A/J mice was poor inducer both CTL and delayed hypersensitivity (DTH) responses. We also followed histologically immunohistochemically course disease following topical (TC) infection with wild (WT) HSV-1, TC gC-39 simultaneous anterior chamber (TC + AC) WT HSV-1. The latter induce profound state DTH tolerance Following progressed severe ulcerative keratitis neovascularization by day 21. Histologic immunohistochemical analysis predominantly mononuclear infiltrate consisting numerous plasma cells as well L3T4+ (T helper/inducer) Lyt-2+ suppressor/cytotoxic) lymphocytes. gC-39, or AC severity did progress beyond 7. On 21, there most mild cellular polymorphonuclear neutrophils. These findings indicate early consists nonspecific inflammatory response, but involves CMI injection inhibits thereby halting progression disease. Similarly, responses, is