Abstract
Purpose: :
Several studies have indicated that the co-stimulatory interaction of CD137 with CD137L plays an important role in the development of anti-viral responses. These studies suggested that this interaction potentiated the development of anti-viral responses involving anti-viral CTL’s and antibody responses. We decided to investigate this interaction using mice deficient in CD137L expression.
Methods: :
CD137L deficient mice along with their B6 controls were infected with the McKrae strain of HSV-1 by corneal scarification. These mice were then observed for the development of acute herpetic keratitis and the development of anti-HSV-1 antibodies.
Results: :
In contrast to what had previously been reported for CD137-/- mice, CD137L-/- mice displayed significantly increased corneal disease as judged by opacity, neovascularization, and blepharitis than was observed in B6 mice. However, these mice did not display increased mortality following infection as a slightly higher percentage of CD137-/- mice survived corneal infection than did B6 mice (58% vs. 44%). Antibody responses, as measured by anti-HSV-1 titers at 4 weeks post-infection were greater in the control B6 mice than were seen in CD137L-/- mice.
Conclusions: :
We conclude from this study that the interaction of CD137 with CD137L is important in the control of HSV-1 induced corneal disease. Furthermore, we suspect that the development of non-inflammatory immune responses maybe the mechanism responsible for this observation.
Keywords: herpes simplex virus • keratitis