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dc.contributor.authorvon Muenchow, Lilly
dc.contributor.authorAlberti-Servera, Llucia
dc.contributor.authorKlein, Fabian
dc.contributor.authorCapoferri, Giuseppina
dc.contributor.authorFinke, Daniela
dc.contributor.authorCeredig, Rhodri
dc.contributor.authorRolink, Antonius
dc.contributor.authorTsapogas, Panagiotis
dc.date.accessioned2017-02-02T13:48:57Z
dc.date.available2017-02-02T13:48:57Z
dc.date.issued2016-11-04
dc.identifier.citationvon Muenchow, Lilly, Alberti-Servera, Llucia, Klein, Fabian, Capoferri, Giuseppina, Finke, Daniela, Ceredig, Rhodri, Rolink, Antonius, Tsapogas, Panagiotis. (2016). Permissive roles of cytokines interleukin-7 and Flt3 ligand in mouse B-cell lineage commitment. Proceedings of the National Academy of Sciences, 113(50), E8122-E8130. doi: 10.1073/pnas.1613316113en_IE
dc.identifier.issn1091-6490
dc.identifier.urihttp://hdl.handle.net/10379/6279
dc.description.abstractHematopoietic cells are continuously generated throughout life from hematopoietic stem cells, thus making hematopoiesis a favorable system to study developmental cell lineage commitment. The main factors incorporating environmental signals to developing hematopoietic cells are cytokines, which regulate commitment of hematopoietic progenitors to the different blood lineages by acting either in an instructive or a permissive manner. Fms-like tyrosine kinase-3 (Flt3) ligand (FL) and Interleukin-7 (IL-7) are cytokines pivotal for B-cell development, as manifested by the severely compromised B-cell development in their absence. However, their precise role in regulating B-cell commitment has been the subject of debate. In the present study we assessed the rescue of B-cell commitment in mice lacking IL-7 but simultaneously overexpressing FL. Results obtained demonstrate that FL overexpression in IL-7–deficient mice rescues B-cell commitment, resulting in significant Ebf1 and Pax5 expression in Ly6D+CD135+CD127+CD19− precursors and subsequent generation of normal numbers of CD19+ B-cell progenitors, therefore indicating that IL-7 can be dispensable for commitment to the B-cell lineage. Further analysis of Ly6D+CD135+CD127+CD19− progenitors in IL-7– or FL-deficient mice overexpressing Bcl2, as well as in IL-7 transgenic mice suggests that both FL and IL-7 regulate B-cell commitment in a permissive manner: FL by inducing proliferation of Ly6D+CD135+CD127+CD19− progenitors and IL-7 by providing survival signals to these progenitors.en_IE
dc.description.sponsorshipA.R. is holder of the chair in immunology (University of Basel) endowed by L. Hoffmann, La Roche Ltd, Basel. This study was supported by the Swiss National Science Foundation and by the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework Programme FP7/2007-2013 under Research Executive Agency Grant 315902. R.C. was supported by Science Foundation Ireland Grants SFI09/SRC/B1794 and SFI07/SK/B1233b.en_IE
dc.formatapplication/pdfen_IE
dc.language.isoenen_IE
dc.publisherNational Academy of Sciencesen_IE
dc.relation.ispartofProceedings Of The National Academy Of Sciences Usaen
dc.subjectHematopoiesisen_IE
dc.subjectCytokinesen_IE
dc.subjectCommitmenten_IE
dc.subjectImmunologyen_IE
dc.subjectMedicineen_IE
dc.titlePermissive roles of cytokines Interleukin-7 and Flt3-ligand in mouse B cell lineage commitmenten_IE
dc.typeArticleen_IE
dc.date.updated2017-01-30T10:58:49Z
dc.identifier.doi10.1073/pnas.1613316113
dc.local.publishedsourcehttp://dx.doi.org/10.1073/pnas.1613316113en_IE
dc.description.peer-reviewedpeer-reviewed
dc.contributor.funder|~|1267872|~|1267880|~|1267883|~|
dc.internal.rssid11774909
dc.local.contactRhodri Ceredig, Room 217, Orbsen Building, Nui Galway. 5916 Email: rhodri.ceredig@nuigalway.ie
dc.local.copyrightcheckedNo
dc.local.versionACCEPTED
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