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dc.contributor.authorRoberts, Luke B; orcid: 0000-0003-1143-304X
dc.contributor.authorJowett, Geraldine M; orcid: 0000-0002-8436-6637
dc.contributor.authorRead, Emily; orcid: 0000-0002-0376-2989
dc.contributor.authorZabinski, Tomas
dc.contributor.authorBerkachy, Rita; orcid: 0000-0002-2053-5913
dc.contributor.authorSelkirk, Murray E; orcid: 0000-0002-6274-6014
dc.contributor.authorJackson, Ian
dc.contributor.authorNiazi, Umar; orcid: 0000-0001-7176-8883
dc.contributor.authorAnandagoda, Nelomi
dc.contributor.authorAraki, Masatake
dc.contributor.authorAraki, Kimi
dc.contributor.authorKasturiarachchi, Jagath
dc.contributor.authorJames, Chela; orcid: 0000-0003-3996-0909
dc.contributor.authorEnver, Tariq
dc.contributor.authorNimmo, Rachael; orcid: 0000-0001-6213-9030
dc.contributor.authorReis, Rita; orcid: 0000-0002-0182-6694
dc.contributor.authorHoward, Jane K; orcid: 0000-0003-2754-8300
dc.contributor.authorNeves, Joana F; orcid: 0000-0001-5842-4162
dc.contributor.authorLord, Graham M; orcid: 0000-0003-2069-4743; email: graham.lord@manchester.ac.uk
dc.date.accessioned2021-06-05T00:57:51Z
dc.date.available2021-06-05T00:57:51Z
dc.date.issued2021-05-21
dc.date.submitted2020-06-01
dc.identifierpubmed: 34021046
dc.identifierpii: jimmunol.2000647
dc.identifierdoi: 10.4049/jimmunol.2000647
dc.identifierpmc: PMC7610861
dc.identifiermid: EMS121076
dc.identifier.citationJournal of immunology (Baltimore, Md. : 1950), volume 206, issue 11, page 2725-2739
dc.identifier.urihttp://hdl.handle.net/10034/624847
dc.descriptionFrom PubMed via Jisc Publications Router
dc.descriptionHistory: received 2020-06-01, accepted 2021-03-19
dc.descriptionPublication status: ppublish
dc.descriptionFunder: Wellcome Trust; Grant(s): 204394
dc.descriptionFunder: British Heart Foundation; Grant(s): PG/12/36/29444
dc.descriptionFunder: Medical Research Council; Grant(s): MR/M003493/1, MR/R024812/1
dc.description.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.]
dc.languageeng
dc.sourceeissn: 1550-6606
dc.titleMicroRNA-142 Critically Regulates Group 2 Innate Lymphoid Cell Homeostasis and Function.
dc.typearticle
dc.date.updated2021-06-05T00:57:51Z
dc.date.accepted2021-03-19


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