MicroRNA-142 Critically Regulates Group 2 Innate Lymphoid Cell Homeostasis and Function.
AuthorsRoberts, Luke B; orcid: 0000-0003-1143-304X
Jowett, Geraldine M; orcid: 0000-0002-8436-6637
Read, Emily; orcid: 0000-0002-0376-2989
Berkachy, Rita; orcid: 0000-0002-2053-5913
Selkirk, Murray E; orcid: 0000-0002-6274-6014
Niazi, Umar; orcid: 0000-0001-7176-8883
James, Chela; orcid: 0000-0003-3996-0909
Nimmo, Rachael; orcid: 0000-0001-6213-9030
Reis, Rita; orcid: 0000-0002-0182-6694
Howard, Jane K; orcid: 0000-0003-2754-8300
Neves, Joana F; orcid: 0000-0001-5842-4162
Lord, Graham M; orcid: 0000-0003-2069-4743; email: email@example.com
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AbstractInnate lymphoid cells are central to the regulation of immunity at mucosal barrier sites, with group 2 innate lymphoid cells (ILC2s) being particularly important in type 2 immunity. In this study, we demonstrate that microRNA(miR)-142 plays a critical, cell-intrinsic role in the homeostasis and function of ILC2s. Mice deficient for miR-142 expression demonstrate an ILC2 progenitor-biased development in the bone marrow, and along with peripheral ILC2s at mucosal sites, these cells display a greatly altered phenotype based on surface marker expression. ILC2 proliferative and effector functions are severely dysfunctional following infection, revealing a critical role for miR-142 isoforms in ILC2-mediated immune responses. Mechanistically, and expression are regulated by miR-142 isoforms in ILC2s, impacting ILC2 phenotypes as well as the proliferative and effector capacity of these cells. The identification of these novel pathways opens potential new avenues to modulate ILC2-dependent immune functions. [Abstract copyright: Copyright © 2021 The Authors.]
CitationJournal of immunology (Baltimore, Md. : 1950), volume 206, issue 11, page 2725-2739
DescriptionFrom PubMed via Jisc Publications Router
History: received 2020-06-01, accepted 2021-03-19
Publication status: ppublish
Funder: Wellcome Trust; Grant(s): 204394
Funder: British Heart Foundation; Grant(s): PG/12/36/29444
Funder: Medical Research Council; Grant(s): MR/M003493/1, MR/R024812/1
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