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dc.contributor.authorParker, David C.
dc.contributor.authorGreiner, Dale L.
dc.contributor.authorPhillips, Nancy E.
dc.contributor.authorAppel, Michael C.
dc.contributor.authorSteele, Alan W.
dc.contributor.authorDurie, Fiona H.
dc.contributor.authorNoelle, Randolph J.
dc.contributor.authorMordes, John P.
dc.contributor.authorRossini, Aldo A.
dc.date2022-08-11T08:09:36.000
dc.date.accessioned2022-08-23T16:37:16Z
dc.date.available2022-08-23T16:37:16Z
dc.date.issued1995-10-10
dc.date.submitted2009-04-02
dc.identifier.citation<p>Proc Natl Acad Sci U S A. 1995 Oct 10;92(21):9560-4.</p>
dc.identifier.issn0027-8424 (Print)
dc.identifier.pmid7568172
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38977
dc.description.abstractCombined treatment with allogeneic small lymphocytes or T-depleted small lymphocytes plus a blocking antibody to CD40 ligand (CD40L) permitted indefinite pancreatic islet allograft survival in 37 of 40 recipients that differed from islet donors at major and minor histocompatibility loci. The effect of the allogeneic small lymphocytes was donor antigen-specific. Neither treatment alone was as effective as combined treatment, although anti-CD40L by itself allowed indefinite islet allograft survival in 40% of recipients. Our interpretation is that small lymphocytes expressing donor antigens in the absence of appropriate costimulatory signals are tolerogenic for alloreactive host cells. Anti-CD40L antibody may prevent host T cells from inducing costimulatory signals in donor lymphocytes or islet grafts.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=7568172&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC40841/
dc.subjectAnimals
dc.subjectAntigens, Differentiation, T-Lymphocyte
dc.subjectCD40 Ligand
dc.subjectCrosses, Genetic
dc.subjectDiabetes Mellitus, Experimental
dc.subject*Graft Survival
dc.subjectIslets of Langerhans Transplantation
dc.subject*Lymphocyte Transfusion
dc.subjectMembrane Glycoproteins
dc.subjectMice
dc.subjectMice, Inbred BALB C
dc.subjectMice, Inbred C3H
dc.subjectMice, Inbred C57BL
dc.subjectTransplantation, Homologous
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleSurvival of mouse pancreatic islet allografts in recipients treated with allogeneic small lymphocytes and antibody to CD40 ligand
dc.typeArticle
dc.source.journaltitleProceedings of the National Academy of Sciences of the United States of America
dc.source.volume92
dc.source.issue21
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/1805
dc.identifier.contextkey808571
html.description.abstract<p>Combined treatment with allogeneic small lymphocytes or T-depleted small lymphocytes plus a blocking antibody to CD40 ligand (CD40L) permitted indefinite pancreatic islet allograft survival in 37 of 40 recipients that differed from islet donors at major and minor histocompatibility loci. The effect of the allogeneic small lymphocytes was donor antigen-specific. Neither treatment alone was as effective as combined treatment, although anti-CD40L by itself allowed indefinite islet allograft survival in 40% of recipients. Our interpretation is that small lymphocytes expressing donor antigens in the absence of appropriate costimulatory signals are tolerogenic for alloreactive host cells. Anti-CD40L antibody may prevent host T cells from inducing costimulatory signals in donor lymphocytes or islet grafts.</p>
dc.identifier.submissionpathoapubs/1805
dc.contributor.departmentDepartment of Medicine, Division of Endocrinology and Metabolism
dc.contributor.departmentDepartment of Medicine, Division of Diabetes
dc.contributor.departmentDepartment of Molecular Genetics and Microbiology
dc.source.pages9560-4


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