English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

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.

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