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Enhanced viral immunoinflammatory lesions in mice lacking IL-23 responses

  • Bumseok Kim
  • , Pranita P. Sarangi
  • , Ahmet Kursat Azkur
  • , Shilpa Deshpande Kaistha
  • , Barry T. Rouse*
  • *Corresponding author for this work
  • University of Tennessee System
  • College of Veterinary Medicine

Research output: Contribution to journalJournal articlepeer-review

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-γ 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.

Original languageEnglish
Pages (from-to)302-312
Number of pages11
JournalMicrobes and Infection
Volume10
Issue number3
DOIs
StatePublished - 2008.03

Keywords

  • Herpes simplex virus
  • IFN-γ
  • IL-12
  • IL-17
  • IL-23
  • Stromal keratitis

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