CD11c depletion severely disrupts Th2 induction and development in vivo

Alexander Phythian-Adams, Peter 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

    Research output: Contribution to journalArticlepeer-review

    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. © 2010 Phythian-Adams et al.
    Original languageEnglish
    Pages (from-to)2089-2096
    Number of pages7
    JournalJournal of Experimental Medicine
    Volume207
    Issue number10
    DOIs
    Publication statusPublished - 27 Sept 2010

    Fingerprint

    Dive into the research topics of 'CD11c depletion severely disrupts Th2 induction and development in vivo'. Together they form a unique fingerprint.

    Cite this