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dc.contributor.authorRowley, Sean Michael
dc.date.accessioned2014-03-04T20:59:59Z
dc.date.available2014-03-04T20:59:59Z
dc.date.issued2012-12
dc.identifier.otherrowley_sean_m_201212_ms
dc.identifier.urihttp://purl.galileo.usg.edu/uga_etd/rowley_sean_m_201212_ms
dc.identifier.urihttp://hdl.handle.net/10724/28595
dc.description.abstractThe protein kinase Tpl2 (MAP3K8) regulates innate inflammatory responses and is being actively pursued for therapeutic inhibition during chronic autoimmunity. Herein, we addressed the contribution of Tpl2 to pro-inflammatory responses of NK cells and macrophages. Despite the Tpl2-dependent regulation of IFNγ secretion by CD4+ T-cells, NK cell IFNγ production, STAT4 expression, and expression of cytotoxic machinery occurred independently of Tpl2. In contrast, tpl2-/- macrophages were functionally defective, as they displayed impaired chemokine and chemokine receptor expression following LPS stimulation and were defective in migrating in vivo to inflamed tissues. Tpl2-/- macrophages were also impaired in their differentiation towards a pro-inflammatory phenotype (M1) while conversely displaying an enhanced anti-inflammatory phenotype (M2). Overall, this work provides additional support for targeting Tpl2, through its effects on macrophage recruitment and differentiation, for the treatment of autoimmunity.
dc.languageeng
dc.publisheruga
dc.rightspublic
dc.subjectautoimmunity
dc.subjectinflammation
dc.subjectcytokines
dc.subjectchemokines
dc.subjectcellular trafficking
dc.subjectNK cells
dc.subjectmacrophage classical activation
dc.subjectmacrophage alternative activation
dc.titleTpl2 (MAP3K8) regulates the migration, differentiation, and function of critical innate immune cells during the inflammatory response
dc.typeThesis
dc.description.degreeMS
dc.description.departmentInfectious Diseases
dc.description.majorVeterinary and Biomedical Sciences
dc.description.advisorWendy Watford
dc.description.committeeWendy Watford
dc.description.committeeLiliana Jaso-Friedmann
dc.description.committeeDonald Harn


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