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Transplantation survival is maintained by granzyme B+ regulatory cells and adaptive regulatory T cells

dc.contributor.authorGondek, David C.
dc.contributor.authorDevries, Victor
dc.contributor.authorNowak, Elizabeth C.
dc.contributor.authorLu, Li-Fan
dc.contributor.authorBennett, Kathryn A.
dc.contributor.authorScott, Zachary Aaron
dc.contributor.authorNoelle, Randolph J.
dc.date2022-08-11T08:08:52.000
dc.date.accessioned2022-08-23T16:10:46Z
dc.date.available2022-08-23T16:10:46Z
dc.date.issued2008-09-20
dc.date.submitted2009-02-25
dc.identifier.citation<p>J Immunol. 2008 Oct 1;181(7):4752-60.</p>
dc.identifier.issn1550-6606 (Electronic)
dc.identifier.doi10.4049/jimmunol.181.7.4752
dc.identifier.pmid18802078
dc.identifier.urihttp://hdl.handle.net/20.500.14038/33009
dc.description.abstractGranzyme B (GZB) has been implicated as an effector mechanism in regulatory T cells (T(reg)) suppression. In a model of T(reg)-dependent graft tolerance, it is shown that GZB- deficient mice are unable to establish long-term tolerance. Moreover, mice overexpressing the inhibitor of GZB, serine protease inhibitor 6, are also resistant to tolerization to alloantigen. Graft survival was shorter in bone marrow-mixed chimeras reconstituted with GZB-deficient T(reg) as compared with wild-type T(reg). Whereas there was no difference in graft survival in mixed chimeras reconstituted with wild-type, perforin-deficient, or Fas ligand-deficient T(reg). Finally, data also show that if alloreactive effectors cannot express FoxP3 and be induced to convert in the presence of competent T(reg), then graft tolerance is lost. Our data are the first in vivo data to implicate GZB expression by T(reg) in sustaining long-lived graft survival.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=18802078&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pubmed/?term=18802078
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleTransplantation survival is maintained by granzyme B+ regulatory cells and adaptive regulatory T cells
dc.typeJournal Article
dc.source.journaltitleJournal of immunology (Baltimore, Md. : 1950)
dc.source.volume181
dc.source.issue7
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/1558
dc.identifier.contextkey740097
html.description.abstract<p>Granzyme B (GZB) has been implicated as an effector mechanism in regulatory T cells (T(reg)) suppression. In a model of T(reg)-dependent graft tolerance, it is shown that GZB- deficient mice are unable to establish long-term tolerance. Moreover, mice overexpressing the inhibitor of GZB, serine protease inhibitor 6, are also resistant to tolerization to alloantigen. Graft survival was shorter in bone marrow-mixed chimeras reconstituted with GZB-deficient T(reg) as compared with wild-type T(reg). Whereas there was no difference in graft survival in mixed chimeras reconstituted with wild-type, perforin-deficient, or Fas ligand-deficient T(reg). Finally, data also show that if alloreactive effectors cannot express FoxP3 and be induced to convert in the presence of competent T(reg), then graft tolerance is lost. Our data are the first in vivo data to implicate GZB expression by T(reg) in sustaining long-lived graft survival.</p>
dc.identifier.submissionpathgsbs_sp/1558
dc.contributor.departmentDepartment of Microbiology and Immunology
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages4752-60


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