Interferon Gamma Mediates Hematopoietic Stem Cell Activation and Niche Relocalization through BST2

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dc.citation.articleNumber108530en_US
dc.citation.issueNumber12en_US
dc.citation.journalTitleCell Reportsen_US
dc.citation.volumeNumber33en_US
dc.contributor.authorFlorez, Marcus A.en_US
dc.contributor.authorMatatall, Katie A.en_US
dc.contributor.authorJeong, Youngjaeen_US
dc.contributor.authorOrtinau, Lauraen_US
dc.contributor.authorShafer, Paul W.en_US
dc.contributor.authorLynch, Anne M.en_US
dc.contributor.authorJaksik, Romanen_US
dc.contributor.authorKimmel, Mareken_US
dc.contributor.authorPark, Dongsuen_US
dc.contributor.authorKing, Katherine Y.en_US
dc.date.accessioned2021-02-08T18:37:43Zen_US
dc.date.available2021-02-08T18:37:43Zen_US
dc.date.issued2020en_US
dc.description.abstractDuring chronic infection, the inflammatory cytokine interferon gamma (IFNγ) damages hematopoietic stem cells (HSCs) by disrupting quiescence and promoting excessive terminal differentiation. However, the mechanism by which IFNγ hinders HSC quiescence remains undefined. Using intravital 3-dimensional microscopy, we find that IFNγ disrupts the normally close interaction between HSCs and CXCL12-abundant reticular (CAR) cells in the HSC niche. IFNγ stimulation increases expression of the cell surface protein BST2, which we find is required for IFNγ-dependent HSC relocalization and activation. IFNγ stimulation of HSCs increases their E-selectin binding by BST2 and homing to the bone marrow, which depends on E-selectin binding. Upon chronic infection, HSCs from mice lacking BST2 are more quiescent and more resistant to depletion than HSCs from wild-type mice. Overall, this study defines a critical mechanism by which IFNγ promotes niche relocalization and activation in response to inflammatory stimulation and identifies BST2 as a key regulator of HSC quiescence.en_US
dc.identifier.citationFlorez, Marcus A., Matatall, Katie A., Jeong, Youngjae, et al.. "Interferon Gamma Mediates Hematopoietic Stem Cell Activation and Niche Relocalization through BST2." <i>Cell Reports,</i> 33, no. 12 (2020) Cell Press: https://doi.org/10.1016/j.celrep.2020.108530.en_US
dc.identifier.digitalInterferonGammaen_US
dc.identifier.doihttps://doi.org/10.1016/j.celrep.2020.108530en_US
dc.identifier.urihttps://hdl.handle.net/1911/109804en_US
dc.language.isoengen_US
dc.publisherCell Pressen_US
dc.rightsThis is an open access article under the CC BY-NC-ND licenseen_US
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/en_US
dc.subject.keywordhematopoietic stem cellen_US
dc.subject.keywordinfectionen_US
dc.subject.keywordinterferon gammaen_US
dc.subject.keywordnicheen_US
dc.subject.keywordhomingen_US
dc.subject.keywordBST2en_US
dc.subject.keywordE-selectinen_US
dc.subject.keywordinflammationen_US
dc.titleInterferon Gamma Mediates Hematopoietic Stem Cell Activation and Niche Relocalization through BST2en_US
dc.typeJournal articleen_US
dc.type.dcmiTexten_US
dc.type.publicationpublisher versionen_US
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