Dendritic-cell expression of Ship1 regulates Th2 immunity to helminth infection in mice

Matthew J. Gold, Frann Antignano, Michael R. Hughes, Colby Zaph, Kelly M. McNagny

Research output: Contribution to journalArticleResearchpeer-review

9 Citations (Scopus)


In mouse models of infection with the gastrointestinal parasite Trichuris muris, appropriate dendritic-cell (DC) Ag sampling, migration, and presentation to T cells are necessary to mount a protective Th2-polarized adaptive immune response, which is needed to clear infection. SH2-containing inositol 5' -phosphatase 1 (SHIP-1) has been shown to be an important regulator of DC function in vitro through the negative regulation of the phosphoinositide 3-kinase (PI3K) pathway, but its role in vivo is relatively unexplored. In the current work, mice with a specific deletion of SHIP-1 in DCs (Ship1ΔDC ) were infected with the parasite T. muris. Ship1ΔDC mice were susceptible to infection due to ineffective priming of Th2-polarized responses. This is likely due to an increased production of interleukin (IL) 12p40 by SHIP-1-deficient DCs, as in vivo antibody blockade of IL-12p40 was able to facilitate the clearing of infection in Ship1ΔDC mice. Our results describe a critical role for SHIP-1 in regulating the ability of DCs to efficiently prime Th2-type responses.
Original languageEnglish
Pages (from-to)122-130
Number of pages9
JournalEuropean Journal of Immunology
Issue number1
Publication statusPublished - Jan 2016


  • dendritic cell
  • P13K
  • SHIP-1
  • Th2
  • trichuris muris

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