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 language | English |
|---|---|
| Pages (from-to) | 302-312 |
| Number of pages | 11 |
| Journal | Microbes and Infection |
| Volume | 10 |
| Issue number | 3 |
| DOIs | |
| State | Published - 2008.03 |
Keywords
- Herpes simplex virus
- IFN-γ
- IL-12
- IL-17
- IL-23
- Stromal keratitis
Fingerprint
Dive into the research topics of 'Enhanced viral immunoinflammatory lesions in mice lacking IL-23 responses'. Together they form a unique fingerprint.Cite this
- APA
- Author
- BIBTEX
- Harvard
- Standard
- RIS
- Vancouver