Cbfβ2 deficiency preserves Langerhans cell precursors by lack of selective TGFβ receptor signaling.

ABSTRACT: The mouse Langerhans cell (LC) network is established through the differentiation of embryonic LC precursors. BMP7 and TGFβ1 initiate cellular signaling that is essential for inducing LC differentiation and preserving LCs in a quiescent state, respectively. Here we show that loss of Cbfβ2, one of two RNA splice variants of the Cbfb gene, results in long-term persistence of embryonic LC precursors after their developmental arrest at the transition into the EpCAM⁺ stage. This phenotype is caused by selective loss of BMP7-mediated signaling essential for LC differentiation, whereas TGFβR signaling is intact, maintaining cells in a quiescent state. Transgenic Cbfβ2 expression at the neonatal stage, but not at the adult stage, restored differentiation from Cbfβ2-deficient LC p

SUBMITTER: Tenno M 

PROVIDER: S-EPMC5626404 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature