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PLoS Pathog. 2009 Oct;5(10):e1000610. doi: 10.1371/journal.ppat.1000610. Epub 2009 Oct 9.

IL-10 signaling blockade controls murine West Nile virus infection.

Author information

1
Section of Infectious Diseases, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, United States of America.

Abstract

West Nile virus (WNV), a mosquito-borne single-stranded RNA flavivirus, can cause significant human morbidity and mortality. Our data show that interleukin-10 (IL-10) is dramatically elevated both in vitro and in vivo following WNV infection. Consistent with an etiologic role of IL-10 in WNV pathogenesis, we find that WNV infection is markedly diminished in IL-10 deficient (IL-10(-/-)) mice, and pharmacologic blockade of IL-10 signaling by IL-10 neutralizing antibody increases survival of WNV-infected mice. Increased production of antiviral cytokines in IL-10(-/-) mice is associated with more efficient control of WNV infection. Moreover, CD4(+) T cells produce copious amounts of IL-10, and may be an important cellular source of IL-10 during WNV infection in vivo. In conclusion, IL-10 signaling plays a negative role in immunity against WNV infection, and blockade of IL-10 signaling by genetic or pharmacologic means helps to control viral infection, suggesting a novel anti-WNV therapeutic strategy.

PMID:
19816558
PMCID:
PMC2749443
DOI:
10.1371/journal.ppat.1000610
[Indexed for MEDLINE]
Free PMC Article

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