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P. M. Stuart, X.-T. Yin; Lack of CD137-CD137L Costimulation is Associated With Increased Corneal Disease Following Infection With HSV-1, McKrae Strain. Invest. Ophthalmol. Vis. Sci. 2010;51(13):3877.
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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.
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.
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.
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.
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