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TGFβR signalling controls CD103+CD11b+ dendritic cell development in the intestine

Author

Listed:
  • C. C. Bain

    (University of Glasgow
    University of Edinburgh)

  • J. Montgomery

    (University of Glasgow)

  • C. L. Scott

    (University of Glasgow
    VIB-UGent Center for Inflammation Research
    Ghent University)

  • J. M. Kel

    (University Medical Center)

  • M. J. H. Girard-Madoux

    (University Medical Center)

  • L. Martens

    (Ghent University
    VIB Inflammation Research Center)

  • T. F. P. Zangerle-Murray

    (University of Glasgow
    University of Manchester)

  • J. Ober-Blöbaum

    (University Medical Center
    University Medical Centre of the Johannes Gutenberg University)

  • D. Lindenbergh-Kortleve

    (Erasmus Medical Center)

  • J. N. Samsom

    (Erasmus Medical Center)

  • S. Henri

    (Aix Marseille Université UM2, INSERM, U1104, CNRS UMR7280)

  • T. Lawrence

    (Aix Marseille Université UM2, INSERM, U1104, CNRS UMR7280)

  • Y. Saeys

    (VIB Inflammation Research Center
    Ghent University)

  • B. Malissen

    (Aix Marseille Université UM2, INSERM, U1104, CNRS UMR7280)

  • M. Dalod

    (Aix Marseille Université UM2, INSERM, U1104, CNRS UMR7280)

  • B. E. Clausen

    (University Medical Center
    University Medical Centre of the Johannes Gutenberg University)

  • A. McI. Mowat

    (University of Glasgow)

Abstract

CD103+CD11b+ dendritic cells (DCs) are unique to the intestine, but the factors governing their differentiation are unclear. Here we show that transforming growth factor receptor 1 (TGFβR1) has an indispensable, cell intrinsic role in the development of these cells. Deletion of Tgfbr1 results in markedly fewer intestinal CD103+CD11b+ DCs and a reciprocal increase in the CD103−CD11b+ dendritic cell subset. Transcriptional profiling identifies markers that define the CD103+CD11b+ DC lineage, including CD101, TREM1 and Siglec-F, and shows that the absence of CD103+CD11b+ DCs in CD11c-Cre.Tgfbr1 fl/fl mice reflects defective differentiation from CD103−CD11b+ intermediaries, rather than an isolated loss of CD103 expression. The defect in CD103+CD11b+ DCs is accompanied by reduced generation of antigen-specific, inducible FoxP3+ regulatory T cells in vitro and in vivo, and by reduced numbers of endogenous Th17 cells in the intestinal mucosa. Thus, TGFβR1-mediated signalling may explain the tissue-specific development of these unique DCs.

Suggested Citation

  • C. C. Bain & J. Montgomery & C. L. Scott & J. M. Kel & M. J. H. Girard-Madoux & L. Martens & T. F. P. Zangerle-Murray & J. Ober-Blöbaum & D. Lindenbergh-Kortleve & J. N. Samsom & S. Henri & T. Lawrenc, 2017. "TGFβR signalling controls CD103+CD11b+ dendritic cell development in the intestine," Nature Communications, Nature, vol. 8(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-00658-6
    DOI: 10.1038/s41467-017-00658-6
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