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dc.contributor.authorJ. Stewart, Trina
dc.contributor.authorJ. Liewehr, David
dc.contributor.authorM. Steinberg, Seth
dc.contributor.authorM. Greeneltch, Kristy
dc.contributor.authorI. Abrams, Scott
dc.date.accessioned2017-05-03T16:13:13Z
dc.date.available2017-05-03T16:13:13Z
dc.date.issued2009
dc.date.modified2013-06-13T23:24:41Z
dc.identifier.issn00221767
dc.identifier.doi10.4049/jimmunol.0804132
dc.identifier.urihttp://hdl.handle.net/10072/47231
dc.description.abstractCD11b Gr-1 -expressing cells, termed myeloid-derived suppressor cells, can mediate immunosuppression and tumor progression. However, the intrinsic molecular events that drive their protumorigenic behavior remain to be elucidated. Although CD11b Gr-1 cells exist at low frequencies in normal mice, it also remains unresolved whether they are biologically distinct from those of tumor-bearing hosts. These objectives were investigated using CD11b Gr-1 cells from both implantable (4T1) and autochthonous (mouse mammary tumor virus-polyomavirus middle T Ag (MMTV-PyMT)) mouse models of mammary carcinoma. Limited variation was observed in the expression of markers associated with immunoregulation between CD11b Gr-1 cells of both tumor models, as well as with their respective controls (Cnt). Despite limited differences in phenotype, tumor-induced CD11b Gr-1 cells were found to produce a more immunosuppressive cytokine profile than that observed by Cnt CD11b Gr-1 cells. Furthermore, when admixed with tumor cells, CD11b Gr-1 cells from tumor-bearing mice significantly enhanced neoplastic growth compared with counterpart cells from Cnt mice. However, the protumorigenic behavior of these tumor-induced CD11b Gr-1 cells was significantly diminished when the expression of IFN regulatory factor 8, a key myeloid-associated transcription factor, was enhanced. The loss of this protumorigenic effect occurred independently of the host immune system and correlated with a CD11b Gr-1 cytokine/chemokine production pattern that resembled cells from nontumor-bearing Cnt mice. Overall, our data indicate that 1) tumor-induced CD11b Gr-1 cells from both cancer models were phenotypically similar, but biologically distinct from their nontumor-bearing counterparts and 2) modulation of IFN regulatory factor 8 levels in tumor-induced CD11b Gr-1 cells can significantly abrogate their protumorigenic behavior, which may have important implications for cancer therapy.
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.languageEnglish
dc.language.isoeng
dc.publisherAmerican Association of Immunologists
dc.publisher.placeUnited States
dc.relation.ispartofstudentpublicationN
dc.relation.ispartofpagefrom117
dc.relation.ispartofpageto128
dc.relation.ispartofissue1
dc.relation.ispartofjournalJournal of Immunology
dc.relation.ispartofvolume183
dc.rights.retentionY
dc.subject.fieldofresearchTumour Immunology
dc.subject.fieldofresearchImmunology
dc.subject.fieldofresearchcode110709
dc.subject.fieldofresearchcode1107
dc.titleModulating the Expression of IFN Regulatory Factor 8 Alters the Protumorigenic Behavior of CD11b+Gr-1+ Myeloid Cells
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.rights.copyrightSelf-archiving of the author-manuscript version is not yet supported by this journal. Please refer to the journal link for access to the definitive, published version or contact the author for more information.
gro.date.issued2009
gro.hasfulltextNo Full Text
gro.griffith.authorStewart, Trina


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