IL-22 Signaling Contributes to West Nile Encephalitis Pathogenesis

Penghua Wang*, Fengwei Bai, Lauren A. Zenewicz, Jianfeng Dai, David Gate, Gong Cheng, Long Yang, Feng Qian, Xiaoling Yuan, Ruth R. Montgomery, Richard A. Flavell, Terrence Town, Erol Fikrig

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

58 Scopus citations


The Th17 cytokine, IL-22, regulates host immune responses to extracellular pathogens. Whether IL-22 plays a role in viral infection, however, is poorly understood. We report here that Il22-/- mice were more resistant to lethal West Nile virus (WNV) encephalitis, but had similar viral loads in the periphery compared to wild type (WT) mice. Viral loads, leukocyte infiltrates, proinflammatory cytokines and apoptotic cells in the central nervous system (CNS) of Il22-/- mice were also strikingly reduced. Further examination showed that Cxcr2, a chemokine receptor that plays a non-redundant role in mediating neutrophil migration, was significantly reduced in Il22-/- compared to WT leukocytes. Expression of Cxcr2 ligands, cxcl1 and cxcl5, was lower in Il22-/- brains than wild type mice. Correspondingly, neutrophil migration from the blood into the brain was attenuated following lethal WNV infection of Il22-/- mice. Our results suggest that IL-22 signaling exacerbates lethal WNV encephalitis likely by promoting WNV neuroinvasion.

Original languageEnglish (US)
Article numbere44153
JournalPloS one
Issue number8
StatePublished - Aug 28 2012
Externally publishedYes

ASJC Scopus subject areas

  • General


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