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

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. Lawrence, Y. Saeys, B. Malissen, M. Dalod, B. E. Clausen () and A. McI. Mowat ()
Additional contact information
C. C. Bain: University of Glasgow
J. Montgomery: University of Glasgow
C. L. Scott: University of Glasgow
J. M. Kel: University Medical Center
M. J. H. Girard-Madoux: University Medical Center
L. Martens: Ghent University
T. F. P. Zangerle-Murray: University of Glasgow
J. Ober-Blöbaum: University Medical Center
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
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
A. McI. Mowat: University of Glasgow

Nature Communications, 2017, vol. 8, issue 1, 1-12

Abstract: 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.

Date: 2017
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DOI: 10.1038/s41467-017-00658-6

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