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Novel reporter mouse reveals constitutive and inflammatory expression of IFN-beta in vivo.

Lienenklaus, Stefan (author)
Cornitescu, Marius (author)
Zietara, Natalia (author)
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Łyszkiewicz, Marcin (author)
Gekara, Nelson (author)
Molecular Immunology, Helmholtz Centre for Infection Research, Braunschweig, Germany
Jabłónska, Jadwiga (author)
Edenhofer, Frank (author)
Rajewsky, Klaus (author)
Bruder, Dunja (author)
Hafner, Martin (author)
Staeheli, Peter (author)
Weiss, Siegfried (author)
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 (creator_code:org_t)
The American Association of Immunologists, 2009
2009
English.
In: Journal of Immunology. - : The American Association of Immunologists. - 0022-1767 .- 1550-6606. ; 183:5, s. 3229-3236
  • Journal article (peer-reviewed)
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  • Type I IFN is a major player in innate and adaptive immune responses. Besides, it is involved in organogenesis and tumor development. Generally, IFN responses are amplified by an autocrine loop with IFN-beta as the priming cytokine. However, due to the lack of sensitive detection systems, where and how type I IFN is produced in vivo is still poorly understood. In this study, we describe a luciferase reporter mouse, which allows tracking of IFN-beta gene induction in vivo. Using this reporter mouse, we reveal strong tissue-specific induction of IFN-beta following infection with influenza or La Crosse virus. Importantly, this reporter mouse also allowed us to visualize that IFN-beta is expressed constitutively in several tissues. As suggested before, low amounts of constitutively produced IFN might maintain immune cells in an activated state ready for a timely response to pathogens. Interestingly, thymic epithelial cells were the major source of IFN-beta under noninflammatory conditions. This relatively high constitutive expression was controlled by the NF Aire and might influence induction of tolerance or T cell development.

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