Kim Bumseok, Sarangi Pranita P, Azkur Ahmet Kursat, Kaistha Shilpa Deshpande, Rouse Barry T
Department of Pathobiology, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996, USA.
Microbes Infect. 2008 Mar;10(3):302-12. doi: 10.1016/j.micinf.2007.12.007. Epub 2007 Dec 23.
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.
单纯疱疹病毒（HSV）感染角膜最终会导致免疫病理损伤（基质性角膜炎——SK），损害视力。本报告显示，HSV感染会导致IL-23上调，但正如在p19基因敲除小鼠中所观察到的那样，如果这种反应未能发生，与野生型（WT）动物相比，病变的严重程度、发病率以及病毒诱导的血管生成水平会显著增加（p<0.05）。p19基因敲除小鼠中较高的疾病严重程度似乎是IL-12反应增强的结果，而IL-12反应增强反过来又导致诱导产生更多产生IFN-γ的CD4(+)T细胞，这些细胞是SK的主要调控者。我们的结果表明，HSV诱导的免疫病理损伤的严重程度可能主要是由IL-12驱动的Th1 T细胞反应所致，而非由IL-23控制的产生IL-17的细胞的作用。
