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TGF-? induces ST2 and programs ILC2 development.


ABSTRACT: The molecular pathways underlying the development of innate lymphoid cells (ILCs) are mostly unknown. Here we show that TGF-? signaling programs the development of ILC2s from their progenitors. Specifically, the deficiency of TGF-? receptor II in bone marrow progenitors results in inefficient development of ILC2s, but not ILC1s or ILC3s. Mechanistically, TGF-? signaling is required for the generation and maintenance of ILC2 progenitors (ILC2p). In addition, TGF-? upregulates the expression of the IL-33 receptor gene Il1rl1 (encoding IL-1 receptor-like 1, also known as ST2) in ILC2p and common helper-like innate lymphoid progenitors (CHILP), at least partially through the MEK-dependent pathway. These findings identify a function of TGF-? in the development of ILC2s from their progenitors.

SUBMITTER: Wang L 

PROVIDER: S-EPMC6946674 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature

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The molecular pathways underlying the development of innate lymphoid cells (ILCs) are mostly unknown. Here we show that TGF-β signaling programs the development of ILC2s from their progenitors. Specifically, the deficiency of TGF-β receptor II in bone marrow progenitors results in inefficient development of ILC2s, but not ILC1s or ILC3s. Mechanistically, TGF-β signaling is required for the generation and maintenance of ILC2 progenitors (ILC2p). In addition, TGF-β upregulates the expression of th  ...[more]

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