期刊
FRONTIERS IN IMMUNOLOGY
卷 8, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2017.01302
关键词
interferon-lambda; intestinal epithelium; interleukin 28 receptor; transcription; gastrointestinal tract
类别
资金
- BMBF (e: Bio) [0316170T]
- Collaborative Research Center (Chronic Infection: Microbial Persistence) [SFB900]
- European Research Training Group [1273]
- German Research Foundation (DFG)
- Hannover Biomedical Research School
- Helmholtz Centre for Infection Research Graduate School
- Deutsche Forschungsgemeinschaft [Ho-2236/12-1, Ho-2236/8-1, Ho-2236/14-1, 1656, 1580]
- Helmholtz-Alberta Initiative, Infectious Diseases Research [HAI-IDRSO-073]
Type I (alpha and beta) and type III (lambda) interferons (IFNs) induce the expression of a large set of antiviral effector molecules via their respective surface membrane receptors. Whereas most cell types respond to type I IFN, type III IFN preferentially acts on epithelial cells and protects mucosal organs such as the lung and gastrointestinal tract. Despite the engagement of different receptor molecules, the type I and type III IFN-induced signaling cascade and upregulated gene profile is thought to be largely identical. Here, we comparatively analyzed the response of gut epithelial cells to IFN-beta and IFN-lambda(2) and identified a set of genes predominantly induced by IFN-lambda(2). We confirm the influence of epithelial cell polarization for enhanced type III receptor expression and demonstrate the induction of predominantly IFN-lambda(2)-induced genes in the gut epithelium in vivo. Our results suggest that IFN-lambda(2) targets the epithelium and induces genes to adjust the antiviral host response to the requirements at mucosal body sites.
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