Treatment of Mice with Anti-CD86 mAb Reduces CD8+T Cell-Mediated CTL Activity and Enhances Ocular Viral Replication in HSV-1-Infected Mice

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

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