Treatment of mice with anti-CD86 mAb reduces CD8+ T cell-mediated CTL activity and enhances ocular viral replication in HSV-1-infected mice

Abstract

Purpose: To determine the relative impact of the CD86 (B7-2) costimulatory molecule in protection against ocular HSV-1 infection.

Methods: BALB/c mice were depleted of CD86 by antibody and depleted mice were examined for their ability to withstand HSV-1 ocular infection. Depleted mice were tested for the presence of virus replication, T-cell activation, survival, and eye disease.

Results: Mice that had been depleted of CD86 had significantly higher titers of HSV-1 in their eyes compared to mock-depleted infected mice. However, the levels of corneal scarring between the two groups of mice were similar. Following ocular infection, the levels of class I MHC-restricted cytotoxic T lymphocytes (CTL) were significantly higher in mock-depleted mice than in CD86-depleted mice. Finally, adoptive transfer of primed CD8(+) T cells but not CD4(+) T cells to CD86-depleted mice resulted in a decrease in peak virus titers in the eyes, such that HSV-1 titers were similar to that of their mock-depleted counterparts.

Conclusions: These data demonstrate an important role for CD86 in the development of CTL and reduction of virus replication in the eyes of HSV-1-infected mice.