Mchedlidze T, Kindermann M, Neves AT, Vöhringer D, Neurath M, Wirtz S (2016)
Publication Type: Journal article
Publication year: 2016
Book Volume: 9
Pages Range: 1384-1394
Journal Issue: 6
DOI: 10.1038/mi.2016.20
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.
APA:
Mchedlidze, T., Kindermann, M., Neves, A.T., Vöhringer, D., Neurath, M., & Wirtz, S. (2016). IL-27 suppresses type 2 immune responses in vivo via direct effects on group 2 innate lymphoid cells. Mucosal Immunology, 9(6), 1384-1394. https://doi.org/10.1038/mi.2016.20
MLA:
Mchedlidze, T., et al. "IL-27 suppresses type 2 immune responses in vivo via direct effects on group 2 innate lymphoid cells." Mucosal Immunology 9.6 (2016): 1384-1394.
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