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dc.contributor.authorBank, Ute
dc.contributor.authorDeiser, Katrin
dc.contributor.authorPlaza-Sirvent, Carlos
dc.contributor.authorOsbelt, Lisa
dc.contributor.authorWitte, Amelie
dc.contributor.authorKnop, Laura
dc.contributor.authorLabrenz, Rebecca
dc.contributor.authorJänsch, Robert
dc.contributor.authorRichter, Felix
dc.contributor.authorBiswas, Aindrila
dc.contributor.authorZenclussen, Ana C
dc.contributor.authorVivier, Eric
dc.contributor.authorRomagnani, Chiara
dc.contributor.authorKühl, Anja A
dc.contributor.authorDunay, Ildiko R
dc.contributor.authorStrowig, Till
dc.contributor.authorSchmitz, Ingo
dc.contributor.authorSchüler, Thomas
dc.date.accessioned2020-03-10T12:58:53Z
dc.date.available2020-03-10T12:58:53Z
dc.date.issued2020-02-26
dc.identifier.citationNat Commun. 2020 Feb 26;11(1):1056. doi: 10.1038/s41467-020-14782-3.en_US
dc.identifier.issn2041-1723
dc.identifier.pmid32103006
dc.identifier.doi10.1038/s41467-020-14782-3
dc.identifier.urihttp://hdl.handle.net/10033/622194
dc.description.abstractNKp46+ innate lymphoid cells (ILC) modulate tissue homeostasis and anti-microbial immune responses. ILC development and function are regulated by cytokines such as Interleukin (IL)-7 and IL-15. However, the ILC-intrinsic pathways translating cytokine signals into developmental programs are largely unknown. Here we show that the anti-apoptotic molecule cellular FLICE-like inhibitory protein (c-FLIP) is crucial for the generation of IL-7/IL-15-dependent NKp46+ ILC1, including conventional natural killer (cNK) cells, and ILC3. Cytokine-induced phosphorylation of signal transducer and activator of transcription 5 (STAT5) precedes up-regulation of c-FLIP, which protects developing NKp46+ ILC from TNF-induced apoptosis. NKp46+ ILC-specific inactivation of c-FLIP leads to the loss of all IL-7/IL-15-dependent NKp46+ ILC, thereby inducing early-onset chronic colitis and subsequently microbial dysbiosis; meanwhile, the depletion of cNK, but not NKp46+ ILC1/3, aggravates experimental colitis. In summary, our data demonstrate a non-redundant function of c-FLIP for the generation of NKp46+ ILC, which protect T/B lymphocyte-sufficient mice from intestinal inflammation.en_US
dc.language.isoenen_US
dc.publisherNature researchen_US
dc.rightsAttribution-NonCommercial-ShareAlike 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.titlec-FLIP is crucial for IL-7/IL-15-dependent NKp46 ILC development and protection from intestinal inflammation in mice.en_US
dc.typeArticleen_US
dc.contributor.departmentHZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.en_US
dc.identifier.journalNature communicationsen_US
refterms.dateFOA2020-03-10T12:58:53Z
dc.source.journaltitleNature communications


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