TGF-β induces ST2 and programs ILC2 development

Li Wang, Jun Tang, Xia Yang, Peter Zanvit, Kairong Cui, Wai Lim Ku, Wenwen Jin, Dunfang Zhang, Nathan Goldberg, Alexander Cain, Bing Ni, Keji Zhao, Yuzhang Wu () and WanJun Chen ()
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Li Wang: National Institute of Dental and Craniofacial Research (NIDCR), National Institutes of Health (NIH)
Jun Tang: National Institute of Dental and Craniofacial Research (NIDCR), National Institutes of Health (NIH)
Xia Yang: National Institute of Dental and Craniofacial Research (NIDCR), National Institutes of Health (NIH)
Peter Zanvit: National Institute of Dental and Craniofacial Research (NIDCR), National Institutes of Health (NIH)
Kairong Cui: National Heart, Lung and Blood Institute (NHLBI), National Institutes of Health (NIH)
Wai Lim Ku: National Heart, Lung and Blood Institute (NHLBI), National Institutes of Health (NIH)
Wenwen Jin: National Institute of Dental and Craniofacial Research (NIDCR), National Institutes of Health (NIH)
Dunfang Zhang: National Institute of Dental and Craniofacial Research (NIDCR), National Institutes of Health (NIH)
Nathan Goldberg: National Institute of Dental and Craniofacial Research (NIDCR), National Institutes of Health (NIH)
Alexander Cain: National Institute of Dental and Craniofacial Research (NIDCR), National Institutes of Health (NIH)
Bing Ni: Third Military Medical University
Keji Zhao: National Heart, Lung and Blood Institute (NHLBI), National Institutes of Health (NIH)
Yuzhang Wu: Third Military Medical University
WanJun Chen: National Institute of Dental and Craniofacial Research (NIDCR), National Institutes of Health (NIH)

Nature Communications, 2020, vol. 11, issue 1, 1-15

Abstract: Abstract 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 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-β in the development of ILC2s from their progenitors.

Date: 2020
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DOI: 10.1038/s41467-019-13734-w

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