FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2008288466> ?p ?o ?g. }

• W2008288466 endingPage "174" @default.
• W2008288466 startingPage "174" @default.
• W2008288466 abstract "382 We have recently demonstrated that T cells obtained from patients with chronic renal allograft dysfunction are primed to recognize and respond to specific donor-derived class II MHC allopeptides in vitro. In experimental animal models, class II MHC allopeptide-specific Th1 clones generated from rejecting animals express restricted TCR Vß repertoire and transfer delayed type hypersensitivity responses in vivo. In this study we generated T cell clones from PBMCs of two human renal transplant recipients; the first patient has chronic allograft dysfunction and the second control patient has stable graft function. Patient 1 received a HLA-DR*0101 mismatched living donor renal allograft and currently has chronic allograft dysfunction (creatinine: 2.9mg/dl) with typical histopathological features of chronic rejection. We have previously demonstrated T cell reactivity to peptide (42-62) of HLA-DR*0101 in this patient. Patient 2 received a HLA-DR*1501 mismatched cadaver renal allograft and currently has stable renal function (creatinine: 1.6mg/dl). Allopeptide reactivity was not detectable to any of 5 HLA-DR*1501 allopeptides on each of three separate occasions in this patient. T cell lines were generated from PBMCs of both patients by repeated stimulation with self APC pulsed allopeptide; peptide (42-62) of HLA-DR*0101 was used for patient 1 and peptide(1-21) of HLA-DR*1501 was used for patient 2. T cell clones were then generated by limiting dilution and were phenotyped using flow cytometric analysis. Culture supernatants were analyzed for cytokine production by ELISA, and the TCR Vß expression was characterized by RT-PCR. T cell clones from patient 1 were found to be CD4+ cells which specifically proliferated to peptide (42-62) of HLA-DR*0101 and which produced IL-2 and IFN-γ after re-stimulation with the peptide. Clones from patient 2 proliferated weakly, yet specifically to peptide (1-21) of HLA-DR*1501 and were found to be CD4+ cells which produced IL-4 and IL-10 after re-stimulation with the peptide. RT-PCR transcript analysis with specific human TCR Vß primers showed that the clones from both patients expressed a restricted TCR Vβ repertoire: 5.2, 8, 9, 13.1 and 13.2 for patient 1, and Vß 4, 6, 13.1, 13.1 and 13.1 for patient 2. The is the first demonstration, at the clonal level, that chronic allograft rejection in humans is associated with the presence of CD4+ MHC allopeptide-specific T cell clones that express a Th1 phenotype. In contrast, MHC allopeptide-specific T cell clones generated in the absence of rejection are associated with a (? protective) Th2 phenotype. Expanding these studies and understanding the mechanisms of immune deviation in humans should yield relevant information on the pathogenesis of chronic allograft rejection, the major clinical problem in organ transplantation." @default.
• W2008288466 created "2016-06-24" @default.
• W2008288466 creator A5005242158 @default.
• W2008288466 creator A5028211848 @default.
• W2008288466 creator A5067268055 @default.
• W2008288466 creator A5071460212 @default.
• W2008288466 creator A5086472692 @default.
• W2008288466 creator A5088583362 @default.
• W2008288466 date "1998-05-01" @default.
• W2008288466 modified "2023-10-16" @default.
• W2008288466 title "CHARACTERIZATION OF MHC ALLOPEPTIDE REACTIVE T CELL CLONES FROM HUMAN RENAL ALLOGRAFT RECIPIENTS" @default.
• W2008288466 doi "https://doi.org/10.1097/00007890-199805131-00380" @default.
• W2008288466 hasPublicationYear "1998" @default.
• W2008288466 type Work @default.
• W2008288466 sameAs 2008288466 @default.
• W2008288466 citedByCount "0" @default.
• W2008288466 crossrefType "journal-article" @default.
• W2008288466 hasAuthorship W2008288466A5005242158 @default.
• W2008288466 hasAuthorship W2008288466A5028211848 @default.
• W2008288466 hasAuthorship W2008288466A5067268055 @default.
• W2008288466 hasAuthorship W2008288466A5071460212 @default.
• W2008288466 hasAuthorship W2008288466A5086472692 @default.
• W2008288466 hasAuthorship W2008288466A5088583362 @default.
• W2008288466 hasBestOaLocation W20082884661 @default.
• W2008288466 hasConcept C126322002 @default.
• W2008288466 hasConcept C137061746 @default.
• W2008288466 hasConcept C147483822 @default.
• W2008288466 hasConcept C159641895 @default.
• W2008288466 hasConcept C188280979 @default.
• W2008288466 hasConcept C19317047 @default.
• W2008288466 hasConcept C202751555 @default.
• W2008288466 hasConcept C203014093 @default.
• W2008288466 hasConcept C207936829 @default.
• W2008288466 hasConcept C2776090121 @default.
• W2008288466 hasConcept C2779067128 @default.
• W2008288466 hasConcept C2780306776 @default.
• W2008288466 hasConcept C2911091166 @default.
• W2008288466 hasConcept C55493867 @default.
• W2008288466 hasConcept C71924100 @default.
• W2008288466 hasConcept C86803240 @default.
• W2008288466 hasConcept C8891405 @default.
• W2008288466 hasConceptScore W2008288466C126322002 @default.
• W2008288466 hasConceptScore W2008288466C137061746 @default.
• W2008288466 hasConceptScore W2008288466C147483822 @default.
• W2008288466 hasConceptScore W2008288466C159641895 @default.
• W2008288466 hasConceptScore W2008288466C188280979 @default.
• W2008288466 hasConceptScore W2008288466C19317047 @default.
• W2008288466 hasConceptScore W2008288466C202751555 @default.
• W2008288466 hasConceptScore W2008288466C203014093 @default.
• W2008288466 hasConceptScore W2008288466C207936829 @default.
• W2008288466 hasConceptScore W2008288466C2776090121 @default.
• W2008288466 hasConceptScore W2008288466C2779067128 @default.
• W2008288466 hasConceptScore W2008288466C2780306776 @default.
• W2008288466 hasConceptScore W2008288466C2911091166 @default.
• W2008288466 hasConceptScore W2008288466C55493867 @default.
• W2008288466 hasConceptScore W2008288466C71924100 @default.
• W2008288466 hasConceptScore W2008288466C86803240 @default.
• W2008288466 hasConceptScore W2008288466C8891405 @default.
• W2008288466 hasIssue "Supplement" @default.
• W2008288466 hasLocation W20082884661 @default.
• W2008288466 hasLocation W20082884662 @default.
• W2008288466 hasOpenAccess W2008288466 @default.
• W2008288466 hasPrimaryLocation W20082884661 @default.
• W2008288466 hasRelatedWork W1562295473 @default.
• W2008288466 hasRelatedWork W1970803003 @default.
• W2008288466 hasRelatedWork W1976217255 @default.
• W2008288466 hasRelatedWork W2030948394 @default.
• W2008288466 hasRelatedWork W2046746146 @default.
• W2008288466 hasRelatedWork W2088225463 @default.
• W2008288466 hasRelatedWork W2167461547 @default.
• W2008288466 hasRelatedWork W2339742492 @default.
• W2008288466 hasRelatedWork W2469596609 @default.
• W2008288466 hasRelatedWork W4205305540 @default.
• W2008288466 hasVolume "65" @default.
• W2008288466 isParatext "false" @default.
• W2008288466 isRetracted "false" @default.
• W2008288466 magId "2008288466" @default.
• W2008288466 workType "article" @default.