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

First Author  Bai F Year  2009
Journal  PLoS Pathog Volume  5
Issue  10 Pages  e1000610
PubMed ID  19816558 Mgi Jnum  J:162907
Mgi Id  MGI:4820498 Doi  10.1371/journal.ppat.1000610
Citation  Bai F, et al. (2009) IL-10 signaling blockade controls murine West Nile virus infection. PLoS Pathog 5(10):e1000610
abstractText  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.
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