Enhanced viral immunoinflammatory lesions in mice lacking IL-23 responses |
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Authors: | Kim Bumseok Sarangi Pranita P Azkur Ahmet Kursat Kaistha Shilpa Deshpande Rouse Barry T |
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Affiliation: | Department of Pathobiology, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996, USA. |
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Abstract: | Herpes simplex virus (HSV) infection of the cornea culminates in an immunopathological lesion (stromal keratitis--SK) that impairs vision. This report shows that HSV infection results in IL-23 up-regulation, but if this response fails to occur, as was noted in p19-/- mice, the severity of lesions, their incidence and the level of viral induced angiogenesis were significantly increased compared to wild-type (WT) animals (p<0.05). The higher disease severity in p19-/- mice appeared to be the consequence of an increased IL-12 response that in turn led to the induction of higher numbers of IFN-gamma producing CD4(+)T cells, the principal orchestrators of SK. Our results indicate that the severity of HSV induced immunopathological lesions may be mainly the consequence of IL-12 driven Th1 T cell reactions rather than the action of IL-17 producing cells controlled by IL-23. |
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