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dc.contributor.advisorHamerman, Jessica Aen_US
dc.contributor.authorBuechler, Matthew Bryanen_US
dc.date.accessioned2014-10-13T16:56:08Z
dc.date.submitted2014en_US
dc.identifier.otherBuechler_washington_0250E_13717.pdfen_US
dc.identifier.urihttp://hdl.handle.net/1773/26104
dc.descriptionThesis (Ph.D.)--University of Washington, 2014en_US
dc.description.abstractThe roles of toll-like receptor and type I interferon signaling in modulating myeloid homeostasis are incompletely defined. Here, we investigate how these factors interact to influence myeloid development in the bone marrow and myeloid cell egress from the bone marrow. The findings described here advance our knowledge of basic immunology and may have clinical applications in the contexts of autoimmunity and infection.en_US
dc.format.mimetypeapplication/pdfen_US
dc.language.isoen_USen_US
dc.rightsCopyright is held by the individual authors.en_US
dc.subjectEmergency Myelopoiesis; Myeloid Development; Plasmacytoid Dendritic Cell; Toll-like Receptor; Type I IFNen_US
dc.subject.otherImmunologyen_US
dc.subject.otherimmunologyen_US
dc.titleType I IFN, Toll-like Receptor Signaling and Myeloid Homeostasisen_US
dc.typeThesisen_US
dc.embargo.termsRestrict to UW for 2 years -- then make Open Accessen_US
dc.embargo.lift2016-10-02T16:56:08Z


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