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dc.contributor.author | Bodega-Mayor, Irene | |
dc.contributor.author | Delgado-Wicke, Pablo | |
dc.contributor.author | Arrabal, Alejandro | |
dc.contributor.author | Alegría-Carrasco, Estíbaliz | |
dc.contributor.author | Nicolao-Gómez, Ana | |
dc.contributor.author | Jaén-Castaño, Marta | |
dc.contributor.author | Espadas, Cristina | |
dc.contributor.author | Dopazo, Ana | |
dc.contributor.author | Martín-Gayo, Enrique | |
dc.contributor.author | Gaspar, María Luisa | |
dc.contributor.author | de Andrés, Belén | |
dc.contributor.author | Fernández-Ruiz, Elena | |
dc.date.accessioned | 2024-07-03T10:26:45Z | |
dc.date.available | 2024-07-03T10:26:45Z | |
dc.date.issued | 2024-04-29 | |
dc.identifier.citation | Cell Mol Life Sci. 2024 Apr 29;81(1):199. | es_ES |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/19934 | |
dc.description.abstract | Tyrosine kinase 2 (TYK2) is involved in type I interferon (IFN-I) signaling through IFN receptor 1 (IFNAR1). This signaling pathway is crucial in the early antiviral response and remains incompletely understood on B cells. Therefore, to understand the role of TYK2 in B cells, we studied these cells under homeostatic conditions and following in vitro activation using Tyk2-deficient (Tyk2-/-) mice. Splenic B cell subpopulations were altered in Tyk2-/- compared to wild type (WT) mice. Marginal zone (MZ) cells were decreased and aged B cells (ABC) were increased, whereas follicular (FO) cells remained unchanged. Likewise, there was an imbalance in transitional B cells in juvenile Tyk2-/- mice. RNA sequencing analysis of adult MZ and FO cells isolated from Tyk2-/- and WT mice in homeostasis revealed altered expression of IFN-I and Toll-like receptor 7 (TLR7) signaling pathway genes. Flow cytometry assays corroborated a lower expression of TLR7 in MZ B cells from Tyk2-/- mice. Splenic B cell cultures showed reduced proliferation and differentiation responses after activation with TLR7 ligands in Tyk2-/- compared to WT mice, with a similar response to lipopolysaccharide (LPS) or anti-CD40 + IL-4. IgM, IgG, IL-10 and IL-6 secretion was also decreased in Tyk2-/- B cell cultures. This reduced response of the TLR7 pathway in Tyk2-/- mice was partially restored by IFNα addition. In conclusion, there is a crosstalk between TYK2 and TLR7 mediated by an IFN-I feedback loop, which contributes to the establishment of MZ B cells and to B cell proliferation and differentiation. | es_ES |
dc.description.sponsorship | This study was supported by Instituto de Salud Carlos III from the Spanish Ministry of Science and Innovation, and the European Regional Development Fund (ISCIII-FEDER) “A way to achieve Europe”, Grants PI19/00096 and PI22/00428 to EF-R and PID2022- 1417540B-I00 for BdA and MLG. PDW and AA were supported by PI19/00096, EAC and ANG by INVESTIGO (Exp. 2022-C23. I01.P03.S0020-0000031) and INVESTIGO CAM (Exp. 09-PIN1- 00015.6/2022) from the Spanish Ministry of Science and Innovation and Comunidad Autónoma de Madrid, respectively, both fnanced by the European Union’s Recovery, Transformation and Resilience Plan and NextGenerationEU, and MJC was supported by Dirección General de Innovación e Investigación Tecnológica de la Comunidad de Madrid (RETARACOVID, Grant P2022/BMD-7274 to EF-R). | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Springer | es_ES |
dc.type.hasVersion | VoR | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | * |
dc.subject.mesh | B-Lymphocytes | es_ES |
dc.subject.mesh | Interferon Type I | es_ES |
dc.subject.mesh | Signal Transduction | es_ES |
dc.subject.mesh | Spleen | es_ES |
dc.subject.mesh | Toll-Like Receptor 7 | es_ES |
dc.subject.mesh | TYK2 Kinase | es_ES |
dc.subject.mesh | Animals | es_ES |
dc.subject.mesh | Mice | es_ES |
dc.subject.mesh | Cell Differentiation | es_ES |
dc.subject.mesh | Cell Proliferation | es_ES |
dc.subject.mesh | Cells, Cultured | es_ES |
dc.subject.mesh | Membrane Glycoproteins | es_ES |
dc.subject.mesh | Mice, Inbred C57BL | es_ES |
dc.subject.mesh | Mice, Knockout | es_ES |
dc.title | Tyrosine kinase 2 modulates splenic B cells through type I IFN and TLR7 signaling. | es_ES |
dc.type | journal article | es_ES |
dc.rights.license | Atribución 4.0 Internacional | * |
dc.identifier.pubmedID | 38683377 | es_ES |
dc.format.volume | 81 | es_ES |
dc.format.number | 1 | es_ES |
dc.format.page | 199 | es_ES |
dc.identifier.doi | 10.1007/s00018-024-05234-y | es_ES |
dc.contributor.funder | Instituto de Salud Carlos III | es_ES |
dc.contributor.funder | Ministerio de Ciencia e Innovación (España) | es_ES |
dc.contributor.funder | Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF) | es_ES |
dc.contributor.funder | Comunidad de Madrid (España) | es_ES |
dc.description.peerreviewed | Sí | es_ES |
dc.identifier.e-issn | 1420-9071 | es_ES |
dc.relation.publisherversion | 10.1007/s00018-024-05234-y | es_ES |
dc.identifier.journal | Cellular and molecular life sciences : CMLS | es_ES |
dc.repisalud.orgCNIC | CNIC::Unidades técnicas::Genómica | es_ES |
dc.repisalud.institucion | CNIC | es_ES |
dc.rights.accessRights | open access | es_ES |