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dc.contributor.authorYounos, İbrahim H.
dc.contributor.authorDafferner, Alicia J.
dc.contributor.authorGülen, Dumrul
dc.contributor.authorBritton, Holly C.
dc.contributor.authorTalmadge, James E.
dc.date.accessioned2022-05-11T14:42:10Z
dc.date.available2022-05-11T14:42:10Z
dc.date.issued2012
dc.identifier.issn1567-5769
dc.identifier.issn1878-1705
dc.identifier.urihttps://doi.org/10.1016/j.intimp.2012.05.002
dc.identifier.urihttps://hdl.handle.net/20.500.11776/9261
dc.description.abstractA stress response can induce myeloid progenitor cell (MPC) proliferation, mobilization, and extramedullary hematopoiesis (EMH) within lymphoid and parenchymal organs. Our studies using in vivo BrdU labeling, Ki-67 IHC staining, and carboxyfluorescein succinimidyl ester (CFSE) adoptive cell transfer revealed that spleens, rather than bone marrow (BM) and peripheral blood (PB), from 4T1 mammary tumor-bearing (TB) mice were the primary site of MPC proliferation. The resultant increase in MPCs was associated with tumor hematopoietic growth factor (GF) transcription, decreased apoptosis, as well as, prolonged survival of splenic MPCs. In naive mice. i.v. injected CFSE-labeled MDSCs (myeloid-derived suppressor cells) initially accumulated in the lungs, while in TB mice, they rapidly sequestered in the spleen. In contrast, a few of the injected MDSCs and leukocytes arrested, proliferated, or accumulated in the marrow, tumor, or PB of TB mice. However, BrdU labeling revealed a significant demargination of proliferating splenic MPCs into the PB. In tumors, despite high GF transcript levels, we found that a high frequency of MDSCs was apoptotic. In summary, tumor growth and cytokines regulate MPC proliferation, trafficking, accumulation, apoptosis, and survival. (C) 2012 Elsevier BM. All rights reserved.en_US
dc.description.sponsorshipNebraska Research Initiative (NRI)en_US
dc.description.sponsorshipThis research was funded by a grant from the Nebraska Research Initiative (NRI), Translation of Biotechnology into the Clinic.en_US
dc.language.isoengen_US
dc.publisherElsevieren_US
dc.identifier.doi10.1016/j.intimp.2012.05.002
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectMDSCen_US
dc.subjectG-CSEen_US
dc.subjectNOS-2en_US
dc.subjectTraffickingen_US
dc.subjectProliferationen_US
dc.subjectTherapeutic Propertiesen_US
dc.subjectImmune Suppressionen_US
dc.subjectMobilizationen_US
dc.subjectExpansionen_US
dc.subjectHeterogeneityen_US
dc.subjectAccumulationen_US
dc.subjectInfiltrationen_US
dc.subjectModulationen_US
dc.subjectSunitiniben_US
dc.subjectSubsetsen_US
dc.titleTumor regulation of myeloid-derived suppressor cell proliferation and traffickingen_US
dc.typearticleen_US
dc.relation.ispartofInternational Immunopharmacologyen_US
dc.departmentFakülteler, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Tıbbi Mikrobiyoloji Ana Bilim Dalıen_US
dc.authorid0000-0002-6328-6056
dc.authorid0000-0002-7792-7459
dc.authorid0000-0002-8711-7820
dc.identifier.volume13en_US
dc.identifier.issue3en_US
dc.identifier.startpage245en_US
dc.identifier.endpage256en_US
dc.institutionauthorGülen, Dumrul
dc.institutionauthorTanrıverdi, Yeliz
dc.institutionauthorKaya, Ayşe Demet
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.authorscopusid35175256600
dc.authorscopusid22834263600
dc.authorscopusid6602366586
dc.authorscopusid55173255200
dc.authorscopusid7005192342
dc.authorwosidTalmadge, James/AAF-7242-2020
dc.authorwosidYounos, Ibrahim H/F-9225-2015
dc.authorwosidGulen, Dumrul/A-5955-2017
dc.identifier.wosWOS:000306037500004en_US
dc.identifier.scopus2-s2.0-84861422421en_US
dc.identifier.pmid22609473en_US


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