Type I interferon is required for T helper (Th) 2 induction by dendritic cells

• Lauren M Webb ^[3] ; Rachel J Lundie ^[4] ; Jessica G Borger ^[7] ; Sheila L Brown ^[6] ; Lisa M Connor ^[8] ; Adam NR Cartwright ^[6] ; Annette M Dougall ^[2] ; Ruud HP Wilbers ^[5] ; Peter C Cook ^[6] ; Lucy H Jackson‐Jones ^[7] ; Alexander T Phythian‐Adams ^[6] ; Cecilia Johansson ^[1] ; Daniel M Davis ^[6] ; Benjamin G Dewals ^[2] ; Franca Ronchese ^[8] ; Andrew S MacDonald ^[6]
  1. [1] Imperial College London

     Imperial College London

     Reino Unido

     
  2. [2] University of Liège

     University of Liège

     Arrondissement de Liège, Bélgica

     
  3. [3] University of Manchester

     University of Manchester

     Reino Unido

     
  4. [4] University of Edinburgh

     University of Edinburgh

     Reino Unido

     
  5. [5] Plant Sciences Department Laboratory of Nematology Wageningen University and Research Centre Wageningen, The Netherlands
  6. [6] Manchester Collaborative Centre for Inflammation Research, University of Manchester,Manchester, United Kingdom
  7. [7] Institute of Immunology and Infection Research Centre for Immunity, Infection and Evolution University of Edinburgh Edinburgh, United Kingdom
  8. [8] Malaghan Institute of Medical Research, Wellington, New Zealand

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• Localización: EMBO journal: European Molecular Biology Organization, ISSN 0261-4189, Vol. 36, Nº. 16, 2017, págs. 2404-2418
• Idioma: inglés
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• Resumen

  • 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.