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IL-15 sustains IL-7R-independent ILC2 and ILC3 development
The signals that maintain tissue-resident innate lymphoid cells (ILC) in different microenvironments are incompletely understood. Here we show that IL-7 receptor (IL-7R) is not strictly required for the development of any ILC subset, as residual cells persist in the small intestinal lamina propria (...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5380969/ https://www.ncbi.nlm.nih.gov/pubmed/28361874 http://dx.doi.org/10.1038/ncomms14601 |
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author | Robinette, Michelle L. Bando, Jennifer K. Song, Wilbur Ulland, Tyler K. Gilfillan, Susan Colonna, Marco |
author_facet | Robinette, Michelle L. Bando, Jennifer K. Song, Wilbur Ulland, Tyler K. Gilfillan, Susan Colonna, Marco |
author_sort | Robinette, Michelle L. |
collection | PubMed |
description | The signals that maintain tissue-resident innate lymphoid cells (ILC) in different microenvironments are incompletely understood. Here we show that IL-7 receptor (IL-7R) is not strictly required for the development of any ILC subset, as residual cells persist in the small intestinal lamina propria (siLP) of adult and neonatal Il7ra(−/−) mice. Il7ra(−/−) ILC2 primarily express an ST2(−) phenotype, but are not inflammatory ILC2. CCR6(+) ILC3, which express higher Bcl-2 than other ILC3, are the most abundant subset in Il7ra(−/−) siLP. All ILC subsets are functionally competent in vitro, and are sufficient to provide enhanced protection to infection with C. rodentium. IL-15 equally sustains wild-type and Il7ra(−/−) ILC survival in vitro and compensates for IL-7R deficiency, as residual ILCs are depleted in mice lacking both molecules. Collectively, these data demonstrate that siLP ILCs are not completely IL-7R dependent, but can persist partially through IL-15 signalling. |
format | Online Article Text |
id | pubmed-5380969 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-53809692017-04-21 IL-15 sustains IL-7R-independent ILC2 and ILC3 development Robinette, Michelle L. Bando, Jennifer K. Song, Wilbur Ulland, Tyler K. Gilfillan, Susan Colonna, Marco Nat Commun Article The signals that maintain tissue-resident innate lymphoid cells (ILC) in different microenvironments are incompletely understood. Here we show that IL-7 receptor (IL-7R) is not strictly required for the development of any ILC subset, as residual cells persist in the small intestinal lamina propria (siLP) of adult and neonatal Il7ra(−/−) mice. Il7ra(−/−) ILC2 primarily express an ST2(−) phenotype, but are not inflammatory ILC2. CCR6(+) ILC3, which express higher Bcl-2 than other ILC3, are the most abundant subset in Il7ra(−/−) siLP. All ILC subsets are functionally competent in vitro, and are sufficient to provide enhanced protection to infection with C. rodentium. IL-15 equally sustains wild-type and Il7ra(−/−) ILC survival in vitro and compensates for IL-7R deficiency, as residual ILCs are depleted in mice lacking both molecules. Collectively, these data demonstrate that siLP ILCs are not completely IL-7R dependent, but can persist partially through IL-15 signalling. Nature Publishing Group 2017-03-31 /pmc/articles/PMC5380969/ /pubmed/28361874 http://dx.doi.org/10.1038/ncomms14601 Text en Copyright © 2017, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Robinette, Michelle L. Bando, Jennifer K. Song, Wilbur Ulland, Tyler K. Gilfillan, Susan Colonna, Marco IL-15 sustains IL-7R-independent ILC2 and ILC3 development |
title | IL-15 sustains IL-7R-independent ILC2 and ILC3 development |
title_full | IL-15 sustains IL-7R-independent ILC2 and ILC3 development |
title_fullStr | IL-15 sustains IL-7R-independent ILC2 and ILC3 development |
title_full_unstemmed | IL-15 sustains IL-7R-independent ILC2 and ILC3 development |
title_short | IL-15 sustains IL-7R-independent ILC2 and ILC3 development |
title_sort | il-15 sustains il-7r-independent ilc2 and ilc3 development |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5380969/ https://www.ncbi.nlm.nih.gov/pubmed/28361874 http://dx.doi.org/10.1038/ncomms14601 |
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