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2 results on '"Ober-Blobaum, J"'

1. TGFβR signalling determines CD103+CD11b+ dendritic cell development in the intestine

Author

Bain, C. C., Montgomery, J., Scott, C L, Kel, J M, Girard-Madoux, M J H, Martens, L, Zangerle-Murray, T F P, Ober-Blobaum, J, Lindenbergh-Kortleve, D, Samsom, J N, Henri, S., Lawrence, T, Saeys, Y, Malissen, B., Dalod, M., Clausen, B E, and Mowat, Alan McI.

Subjects
TheoryofComputation_ANALYSISOFALGORITHMSANDPROBLEMCOMPLEXITY, chemical and pharmacologic phenomena, hemic and immune systems
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.

Published
2017

2. TGF beta R signalling controls CD103(+)CD11b(+) dendritic cell development in the intestine

Author

Bain, C. C., Montgomery, J., Scott, C. L., Kel, J. M., Girard-Madoux, M. J. H., Martens, L., Zangerle-Murray, T. F. P., Ober-Blobaum, J., Lindenbergh-Kortleve, D., Samsom, J. N., Henri, S., Lawrence, T., Saeys, Y., Malissen, Bernard, Dalod, M., Clausen, B. E., Mowat, A. Mcl., Immunology, Pediatrics, University of Glasgow, Centre d'Immunologie de Marseille - Luminy (CIML), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU), Erasmus University Medical Center [Rotterdam] (Erasmus MC), Universiteit Gent = Ghent University [Belgium] (UGENT), Department of Applied Mathematics and Computer Science [Ghent], Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and Universiteit Gent = Ghent University (UGENT)

Subjects
[SDV.IMM]Life Sciences [q-bio]/Immunology, chemical and pharmacologic phenomena, hemic and immune systems
Abstract

International audience; 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 (TGF beta beta R1) 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, TGF beta R1-mediated signalling may explain the tissue-specific development of these unique DCs.

Published
2017

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