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CD11c depletion severely disrupts Th2 induction and development in vivo

Research output: Contribution to journalJournal articlepeer-review

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  • Alexander T Phythian-Adams
  • Peter C Cook
  • Rachel J Lundie
  • Lucy H Jones
  • Katherine A Smith
  • Tom A Barr
  • Kristin Hochweller
  • Stephen M Anderton
  • Günter J Hämmerling
  • Rick M Maizels
  • Andrew S MacDonald
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<mark>Journal publication date</mark>27/09/2010
<mark>Journal</mark>The Journal of experimental medicine
Issue number10
Volume207
Number of pages8
Pages (from-to)2089-2096
Publication StatusPublished
Early online date6/09/10
<mark>Original language</mark>English

Abstract

Although dendritic cells (DCs) are adept initiators of CD4(+) T cell responses, their fundamental importance in this regard in Th2 settings remains to be demonstrated. We have used CD11c-diphtheria toxin (DTx) receptor mice to deplete CD11c(+) cells during the priming stage of the CD4(+) Th2 response against the parasitic helminth Schistosoma mansoni. DTx treatment significantly depleted CD11c(+) DCs from all tissues tested, with 70-80% efficacy. Even this incomplete depletion resulted in dramatically impaired CD4(+) T cell production of Th2 cytokines, altering the balance of the immune response and causing a shift toward IFN-γ production. In contrast, basophil depletion using Mar-1 antibody had no measurable effect on Th2 induction in this system. These data underline the vital role that CD11c(+) antigen-presenting cells can play in orchestrating Th2 development against helminth infection in vivo, a response that is ordinarily balanced so as to prevent the potentially damaging production of inflammatory cytokines.