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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

IL-12 deficiency transiently improves viral clearance during the late phase of respiratory tract infection with influenza A virus in mice.

T helper 1-driven immune responses have been implicated in protective immunity against viral infections. Interleukin (IL)-12 is a heterodimeric proinflammatory cytokine formed by a p35 and a p40 subunit that can induce differentiation of naïve T cells towards a T helper 1-response. To determine the role of IL-12 in respiratory tract infection with influenza, p35 gene deficient (p35-/-) and normal wild type mice were intranasally infected with influenza A virus. IL-12 p35-/- mice displayed a transiently enhanced rather than an impaired viral clearance, as indicated by a 10-fold reduction in viral loads on day 8 after infection. Although interferon-gamma levels were significantly lower in the lungs of IL-12 p35-/- mice, their cellular immune responses were not altered, as reflected by similar T cell CD69 expression and influenza-specific T cell recruitment. Our data indicate that endogenous IL-12 impairs viral clearance during the late phase of influenza A virus infection in mice.[1]

References

  1. IL-12 deficiency transiently improves viral clearance during the late phase of respiratory tract infection with influenza A virus in mice. van der Sluijs, K.F., van Elden, L.J., Xiao, Y., Arens, R., Nijhuis, M., Schuurman, R., Florquin, S., Jansen, H.M., Lutter, R., van der Poll, T. Antiviral Res. (2006) [Pubmed]
 
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