期刊
NATURE COMMUNICATIONS
卷 6, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms8090
关键词
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资金
- Wellcome Trust
- Cancer Research UK
- Department of Health via the National Institute for Health Research (NIHR) comprehensive Biomedical Research Centre award
- Marie Curie and EMBO fellowships
- Wellcome Trust [106292/Z/14/Z] Funding Source: Wellcome Trust
- Cancer Research UK [15689, 19309] Funding Source: researchfish
- The Francis Crick Institute [10093, 10136, 10002] Funding Source: researchfish
- Wellcome Trust [106292/Z/14/Z] Funding Source: researchfish
Unrelenting environmental challenges to the gut epithelium place particular demands on the local immune system. In this context, intestinal intraepithelial lymphocytes (IEL) compose a large, highly conserved T cell compartment, hypothesized to provide a first line of defence via cytolysis of dysregulated intestinal epithelial cells (IEC) and cytokine-mediated re-growth of healthy IEC. Here we show that one of the most conspicuous impacts of activated IEL on IEC is the functional upregulation of antiviral interferon (IFN)-responsive genes, mediated by the collective actions of IFNs with other cytokines. Indeed, IEL activation in vivo rapidly provoked type I/III IFN receptor-dependent upregulation of IFN-responsive genes in the villus epithelium. Consistent with this, activated IEL mediators protected cells against virus infection in vitro, and pre-activation of IEL in vivo profoundly limited norovirus infection. Hence, intraepithelial T cell activation offers an overt means to promote the innate antiviral potential of the intestinal epithelium.
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