Type I IFN Induction via Poly-ICLC Protects XXXX against @entity1328 .

@entity1 @entity32 @entity26438 @entity1712 @entity59 @entity19 @entity1327 @entity645 @entity1961 @entity364 @entity14851 @entity1328 @entity15905 @entity68243 @entity636 @entity791
@entity1327 is the most common cause of @entity364 in @entity791 @entity1 . Depletion of @entity1961 cells, such as occurs during advanced @entity791 , is known to be a critical risk factor for developing @entity1328 . However, the role of @entity645 -induced innate @entity32 in susceptibility to @entity1328 has not been evaluated. Thus, we sought to determine the role of Type I IFN induction in host defense against cryptococci by treatment of @entity1327 (H99) infected @entity19 with @entity26438 ( @entity26438 ), a dsRNA virus mimic. Unexpectedly, @entity26438 treatment greatly extended survival of infected @entity19 and reduced fungal burdens in the brain. Protection from @entity1328 by @entity26438 -induced Type I IFN was mediated by @entity68243 rather than @entity15905 . @entity26438 treatment induced a large, rapid and sustained influx of neutrophils and Ly6Chigh monocytes into the lung while suppressing the development of @entity1712 . The @entity26438 -mediated protection against H99 was @entity1961 T cell dependent and analysis of @entity1961 T cell polyfunctionality showed a reduction in @entity59 producing @entity1961 T cells, marginal increases in Th1 cells and dramatic increases in RORyt+ Th17 cells in @entity26438 treated @entity19 . Moreover, the protective effect of @entity26438 against H99 was diminished in IFNy KO @entity19 and by @entity636 neutralization with blocking mAbs. Furthermore, @entity26438 treatment also significantly extended survival of @entity14851 infected @entity19 with reduced fungal loads in the lungs. These data demonstrate that induction of type I IFN dramatically improves host resistance against the etiologic agents of @entity1328 by beneficial alterations in both innate and adaptive immune responses.
