Final published version
Licence: CC BY: Creative Commons Attribution 4.0 International License
Research output: Contribution to Journal/Magazine › Journal article › peer-review
Research output: Contribution to Journal/Magazine › Journal article › peer-review
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TY - JOUR
T1 - Type I interferon is required for T helper (Th) 2 induction by dendritic cells
AU - Webb, Lauren M
AU - Lundie, Rachel J
AU - Borger, Jessica G
AU - Brown, Sheila L
AU - Connor, Lisa M
AU - Cartwright, Adam Nr
AU - Dougall, Annette M
AU - Wilbers, Ruud Hp
AU - Cook, Peter C
AU - Jackson-Jones, Lucy H
AU - Phythian-Adams, Alexander T
AU - Johansson, Cecilia
AU - Davis, Daniel M
AU - Dewals, Benjamin G
AU - Ronchese, Franca
AU - MacDonald, Andrew S
N1 - © 2017 The Authors. Published under the terms of the CC BY 4.0 license.
PY - 2017/8/15
Y1 - 2017/8/15
N2 - 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.
AB - 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.
KW - Allergens
KW - Animals
KW - Dendritic Cells
KW - Interferon Type I
KW - Mice
KW - Mice, Knockout
KW - Pyroglyphidae
KW - Receptor, Interferon alpha-beta
KW - Schistosoma mansoni
KW - Th2 Cells
KW - Journal Article
KW - Research Support, N.I.H., Extramural
KW - Research Support, Non-U.S. Gov't
U2 - 10.15252/embj.201695345
DO - 10.15252/embj.201695345
M3 - Journal article
C2 - 28716804
VL - 36
SP - 2404
EP - 2418
JO - EMBO Journal
JF - EMBO Journal
SN - 0261-4189
IS - 16
ER -