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Mucosal Immunol. 2016 Nov;9(6):1384-1394. doi: 10.1038/mi.2016.20. Epub 2016 Mar 16.

IL-27 suppresses type 2 immune responses in vivo via direct effects on group 2 innate lymphoid cells.

Author information

1
Department of Medicine 1, University Medical Center, Friedrich-Alexander-University, Erlangen-Nuremberg, Germany.
2
Department of Infection Biology, University Medical Center, Friedrich-Alexander-University, Erlangen-Nuremberg, Germany.

Abstract

Group 2 innate lymphoid cells (ILC2) were recently characterized by their ability to produce significant amounts of type-2 signature cytokines and drive central beneficial and pathological features of type-2 immune responses. Although factors such as IL-33 and IL-25 were shown to have ILC2 activating capacity, it is not well understood, how ILC2 responses are regulated in vivo. Here we provide compelling evidence that IL-27-signalling directly inhibits ILC2 responses and reveal a novel mechanism for negative regulation of the innate arm of type-2 immunity. We demonstrate that IL-27-deficiency is linked to increased mucosal presence of ILC2 in a model of inflammatory lung disease. Moreover, IL-27-treatment inhibited ILC2 proliferation and cytokine production and significantly reduced their accumulation in vivo. During helminth infection, regulation of ILC2 by IL-27 directly impacted anti-parasitic immunity. Thus, therapeutic modulation of the IL-27/IL-27R axis may be relevant in a number of inflammatory conditions associated with dysregulated type-2 responses.

PMID:
26982595
DOI:
10.1038/mi.2016.20
[Indexed for MEDLINE]

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