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IFN-α primes T- and NK-cells for IL-15-mediated signaling and cytotoxicity
- Source :
- Hansen , M L , Woetmann , A , Krejsgaard , T , Kopp , K L M , Søkilde , R , Litman , T , Straten , P T , Geisler , C , Wasik , M A , Ødum , N & Eriksen , K W 2011 , ' IFN-α primes T- and NK-cells for IL-15-mediated signaling and cytotoxicity ' , Molecular Immunology , vol. 48 , no. 15-16 , pp. 2087-93 .
- Publication Year :
- 2011
-
Abstract
- Recently it has become clear that interferon (IFN)-α, a type I interferon produced rapidly in response to infection, not only plays a key role in innate immunity, but also promotes adaptive immune responses by influencing the production or function of other cytokines. During infections IFN-α fosters the production of IL-15, which plays a pivotal role in the development, survival and function of NK cells and recruitment and activation of T cells. Since these two cytokines exert overlapping functions during infections, this investigation was undertaken to study the priming effect of IFN-α on the effect of IL-15 on human T and NK cells. We show that IFN-α induces an increased expression of IL-15Rα in human activated peripheral T cells, and in CD8(+) and CD4(+) T-cell lines. Functionally, the IFN-α-enhanced IL-15Rα expression resulted in an enhanced IL-15-mediated phosphorylation of STAT5 and STAT3 followed by a further increase in IL-15Rα expression. Moreover, IFN-α significantly increased the IL-15-induced cytotoxic activity of freshly isolated T and NK cells. Taken together, our data show that IFN-α boosts signaling and functional effects of IL-15, at least in part by fostering the increased IL-15R expression, thus add new facet to the emerging role of IFN-α as an important primer of adaptive immune responses.
Details
- Database :
- OAIster
- Journal :
- Hansen , M L , Woetmann , A , Krejsgaard , T , Kopp , K L M , Søkilde , R , Litman , T , Straten , P T , Geisler , C , Wasik , M A , Ødum , N & Eriksen , K W 2011 , ' IFN-α primes T- and NK-cells for IL-15-mediated signaling and cytotoxicity ' , Molecular Immunology , vol. 48 , no. 15-16 , pp. 2087-93 .
- Notes :
- English
- Publication Type :
- Electronic Resource
- Accession number :
- edsoai.ocn885011711
- Document Type :
- Electronic Resource