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TGF-β induces ST2 and programs ILC2 development
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 develo...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6946674/ https://www.ncbi.nlm.nih.gov/pubmed/31911623 http://dx.doi.org/10.1038/s41467-019-13734-w |
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author | Wang, Li Tang, Jun Yang, Xia Zanvit, Peter Cui, Kairong Ku, Wai Lim Jin, Wenwen Zhang, Dunfang Goldberg, Nathan Cain, Alexander Ni, Bing Zhao, Keji Wu, Yuzhang Chen, WanJun |
author_facet | Wang, Li Tang, Jun Yang, Xia Zanvit, Peter Cui, Kairong Ku, Wai Lim Jin, Wenwen Zhang, Dunfang Goldberg, Nathan Cain, Alexander Ni, Bing Zhao, Keji Wu, Yuzhang Chen, WanJun |
author_sort | Wang, Li |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-6946674 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-69466742020-01-09 TGF-β induces ST2 and programs ILC2 development Wang, Li Tang, Jun Yang, Xia Zanvit, Peter Cui, Kairong Ku, Wai Lim Jin, Wenwen Zhang, Dunfang Goldberg, Nathan Cain, Alexander Ni, Bing Zhao, Keji Wu, Yuzhang Chen, WanJun Nat Commun Article 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. Nature Publishing Group UK 2020-01-07 /pmc/articles/PMC6946674/ /pubmed/31911623 http://dx.doi.org/10.1038/s41467-019-13734-w Text en © This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Wang, Li Tang, Jun Yang, Xia Zanvit, Peter Cui, Kairong Ku, Wai Lim Jin, Wenwen Zhang, Dunfang Goldberg, Nathan Cain, Alexander Ni, Bing Zhao, Keji Wu, Yuzhang Chen, WanJun TGF-β induces ST2 and programs ILC2 development |
title | TGF-β induces ST2 and programs ILC2 development |
title_full | TGF-β induces ST2 and programs ILC2 development |
title_fullStr | TGF-β induces ST2 and programs ILC2 development |
title_full_unstemmed | TGF-β induces ST2 and programs ILC2 development |
title_short | TGF-β induces ST2 and programs ILC2 development |
title_sort | tgf-β induces st2 and programs ilc2 development |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6946674/ https://www.ncbi.nlm.nih.gov/pubmed/31911623 http://dx.doi.org/10.1038/s41467-019-13734-w |
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