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http://hdl.handle.net/2445/209280
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DC Field | Value | Language |
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dc.contributor.author | Umeshappa, Channakeshava Sokke | - |
dc.contributor.author | Solé, Patricia | - |
dc.contributor.author | Yamanouchi, Jun | - |
dc.contributor.author | Mohapatra, Saswat | - |
dc.contributor.author | Surewaard, Bas G. J. | - |
dc.contributor.author | Garnica Caparrós, Josep | - |
dc.contributor.author | Singha, Santiswarup | - |
dc.contributor.author | Mondal, Debajyoti | - |
dc.contributor.author | Cortés Vicente, Elena | - |
dc.contributor.author | D'Mello, Charlotte | - |
dc.contributor.author | Mason, Andrew | - |
dc.contributor.author | Kubes, Paul | - |
dc.contributor.author | Serra, Pau | - |
dc.contributor.author | Yang, Yang | - |
dc.contributor.author | Santamaria, Pere | - |
dc.date.accessioned | 2024-03-27T09:10:54Z | - |
dc.date.available | 2024-03-27T09:10:54Z | - |
dc.date.issued | 2022-06-07 | - |
dc.identifier.issn | 2041-1723 | - |
dc.identifier.uri | http://hdl.handle.net/2445/209280 | - |
dc.description.abstract | Invariant NKT (iNKT) cells comprise a heterogeneous group of non-circulating, tissue-resident T lymphocytes that recognize glycolipids, including alpha-galactosylceramide (?GalCer), in the context of CD1d, but whether peripheral iNKT cell subsets are terminally differentiated remains unclear. Here we show that mouse and human liver-resident ?GalCer/CD1d-binding iNKTs largely correspond to a novel Zbtb16+Tbx21+Gata3+MaflowRorc- subset that exhibits profound transcriptional, phenotypic and functional plasticity. Repetitive in vivo encounters of these liver iNKT (LiNKT) cells with intravenously delivered ?GalCer/CD1d-coated nanoparticles (NP) trigger their differentiation into immunoregulatory, IL-10+IL-21-producing Zbtb16highMafhighTbx21+Gata3+Rorc- cells, termed LiNKTR1, expressing a T regulatory type 1 (TR1)-like transcriptional signature. This response is LiNKT-specific, since neither lung nor splenic tissue-resident iNKT cells from ?GalCer/CD1d-NP-treated mice produce IL-10 or IL-21. Additionally, these LiNKTR1 cells suppress autoantigen presentation, and recognize CD1d expressed on conventional B cells to induce IL-10+IL-35-producing regulatory B (Breg) cells, leading to the suppression of liver and pancreas autoimmunity. Our results thus suggest that LiNKT cells are plastic for further functional diversification, with such plasticity potentially targetable for suppressing tissue-specific inflammatory phenomena.© 2022. The Author(s). | - |
dc.format.extent | 19 p. | - |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | Springer Science and Business Media LLC | - |
dc.relation.isformatof | Reproducció del document publicat a: https://doi.org/10.1038/s41467-022-30759-w | - |
dc.relation.ispartof | Nature Communications, 2022, vol. 13, num. 1 | - |
dc.relation.uri | https://doi.org/10.1038/s41467-022-30759-w | - |
dc.rights | cc by (c) Umeshappa, Channakeshava Sokke et al., 2022 | - |
dc.rights.uri | http://creativecommons.org/licenses/by/3.0/es/ | * |
dc.source | Articles publicats en revistes (IDIBAPS: Institut d'investigacions Biomèdiques August Pi i Sunyer) | - |
dc.subject.classification | Malalties autoimmunitàries | - |
dc.subject.classification | Cèl·lules T | - |
dc.subject.other | Autoimmune diseases | - |
dc.subject.other | T cells | - |
dc.title | Re-programming mouse liver-resident invariant natural killer T cells for suppressing hepatic and diabetogenic autoimmunity | - |
dc.type | info:eu-repo/semantics/article | - |
dc.type | info:eu-repo/semantics/publishedVersion | - |
dc.date.updated | 2023-06-28T08:24:22Z | - |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | - |
dc.identifier.idimarina | 9315830 | - |
dc.identifier.pmid | 35672409 | - |
Appears in Collections: | Articles publicats en revistes (IDIBAPS: Institut d'investigacions Biomèdiques August Pi i Sunyer) |
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File | Description | Size | Format | |
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Re-programming mouse liver-resident invariant natural killer T cells for suppressing hepatic_NatureCommunications.pdf | 5.21 MB | Adobe PDF | View/Open |
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