期刊
EMBO JOURNAL
卷 36, 期 16, 页码 2404-2418出版社
WILEY
DOI: 10.15252/embj.201695345
关键词
dendritic cell; interferon; priming; Th2
资金
- MRC [G0701437, G0800311]
- Wellcome Trust [WT086628MA]
- National Health and Medical Research Council of Australia (NHMRC)
- Health Research Council of New Zealand
- ULg-Marie Curie COFUND Program
- [HHSN272201000005I]
- Asthma UK [MRC-Asthma UK Centre, MRC-AsthmaUKCentre] Funding Source: researchfish
- Medical Research Council [G0701437, G1000758, G1000758B, G0800311] Funding Source: researchfish
- MRC [G0701437, G0800311] Funding Source: UKRI
Type 2 inflammation is a defining feature of infection with parasitic worms (helminths), as well as being responsible for widespread suffering in allergies. However, the precise mechanisms involved in T helper (Th) 2 polarization by dendritic cells (DCs) are currently unclear. We have identified a previously unrecognized role for type I IFN (IFN-I) in enabling this process. An IFN-I signature was evident in DCs responding to the helminth Schistosoma mansoni or the allergen house dust mite (HDM). Further, IFN-I signaling was required for optimal DC phenotypic activation in response to helminth antigen (Ag), and efficient migration to, and localization with, T cells in the draining lymph node (dLN). Importantly, DCs generated from Ifnar1(-/-) mice were incapable of initiating Th2 responses in vivo. These data demonstrate for the first time that the influence of IFN-I is not limited to antiviral or bacterial settings but also has a central role to play in DC initiation of Th2 responses.
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