Mechanisms of immune dysfunction in stem cell transplantation

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dc.authorscopusid7005192342
dc.authorscopusid16212251300
dc.authorscopusid22134581800
dc.authorscopusid6603446778
dc.authorscopusid7004682700
dc.contributor.authorTalmadge J.E.
dc.contributor.authorSingh R.
dc.contributor.authorIno K.
dc.contributor.authorAgeitos A.
dc.contributor.authorBuyukberber S.
dc.date.accessioned2024-08-04T19:59:17Z
dc.date.available2024-08-04T19:59:17Z
dc.date.issued2000
dc.departmentİnönü Üniversitesien_US
dc.description.abstractHigh dose therapy (HDT) and stem cell transplantation (SCT) results in alterations in the immunologic network, thymic re-education and the induction of peripheral tolerance. The changes to the immunoregulatory cascade and tolerance induction associated with autotransplants have been investigated in a series of studies focused on leukocyte reconstitution and function following HDT and autologous SCT. In these studies, we observed a significant decrease in the CD4:CD8 T cell ratio post-transplantation compared to normal peripheral blood (PB) donors due to a decrease in CD4+ cells. In addition, T cell function (phytohemagglutinin (PHA) mitogenesis) was consistently depressed compared to samples obtained from normal PB donors. The loss of T cell function was associated with an increased frequency of circulating monocytes, their expression of Fas ligand (FasL) and a high frequency of apoptotic CD4+ T cells. Indeed, 28-51% of circulating CD4+ T cells were observed to be apoptotic during the first 100 days following HDT and SCT. These studies suggest that 'primed' or activated Fas+ CD4+ lymphocytes interact with FasL+ monocytes, resulting in apoptosis, leading to the preferential deletion of CD4+ T cells, a decrease in the CD4:CD8 T cell ratio and depressed T cell function. Further, as discussed herein, the T cells are activated with a predominantly type 2 phenotype, which may also contribute to the maintenance of the immunosuppressive condition. Therefore, there is the potential to regulate immune recovery by stem cell product manipulation or post-transplantation cytokine administration. © 2000 International Society for Immunopharmacology.en_US
dc.description.sponsorshipNational Institutes of Health; National Cancer Institute, NCI: R01CA061593en_US
dc.description.sponsorshipSource of support: JE Talmadge, NIH Grant RO1-CA61593.en_US
dc.identifier.doi10.1016/S0192-0561(00)00078-3
dc.identifier.endpage1056en_US
dc.identifier.issn0192-0561
dc.identifier.issue12en_US
dc.identifier.pmid11137611en_US
dc.identifier.scopus2-s2.0-0034537473en_US
dc.identifier.scopusqualityN/Aen_US
dc.identifier.startpage1041en_US
dc.identifier.urihttps://doi.org/10.1016/S0192-0561(00)00078-3
dc.identifier.urihttps://hdl.handle.net/11616/90529
dc.identifier.volume22en_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.relation.ispartofInternational Journal of Immunopharmacologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectImmune regulationen_US
dc.subjectPeripheral toleranceen_US
dc.subjectT cell functionen_US
dc.titleMechanisms of immune dysfunction in stem cell transplantationen_US
dc.typeArticleen_US

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