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Plasmacytoid Dendritic Cells Facilitate Th Cell Cytokine Responses throughout Schistosoma mansoni Infection

Research output: Contribution to Journal/MagazineJournal articlepeer-review

  • L.M. Webb
  • A.T. Phythian-Adams
  • A.H. Costain
  • S.L. Brown
  • R.J. Lundie
  • J. Forde-Thomas
  • P.C. Cook
  • L.H. Jackson-Jones
  • A.K. Marley
  • H.H. Smits
  • K.F. Hoffmann
  • E.D. Tait Wojno
  • A.S. MacDonald
<mark>Journal publication date</mark>30/08/2021
Issue number8
Number of pages12
Pages (from-to)721-732
Publication StatusPublished
<mark>Original language</mark>English


Plasmacytoid dendritic cells (pDCs) are potent producers of type I IFN (IFN-I) during viral infection and respond to IFN-I in a positive feedback loop that promotes their function. IFN-I shapes dendritic cell responses during helminth infection, impacting their ability to support Th2 responses. However, the role of pDCs in type 2 inflammation is unclear. Previous studies have shown that pDCs are dispensable for hepatic or splenic Th2 responses during the early stages of murine infection with the trematode Schistosoma mansoni at the onset of parasite egg laying. However, during S. mansoni infection, an ongoing Th2 response against mature parasite eggs is required to protect the liver and intestine from acute damage and how pDCs participate in immune responses to eggs and adult worms in various tissues beyond acute infection remains unclear. We now show that pDCs are required for optimal Th2 cytokine production in response to S. mansoni eggs in the intestinal-draining mesenteric lymph nodes throughout infection and for egg-specific IFN-g at later time points of infection. Further, pDC depletion at chronic stages of infection led to increased hepatic and splenic pathology as well as abrogated Th2 cell cytokine production and activation in the liver. In vitro, mesenteric lymph node pDCs