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• W2155322523 endingPage "135" @default.
• W2155322523 startingPage "129" @default.
• W2155322523 abstract "CTLA-4·Fas ligand (CTLA-4·FasL), a paradigmatic ‘trans signal converter protein (TSCP)’, can attach to APC (via CTLA-4 binding to B7) and direct intercellular inhibitory signals to responding T cells (via FasL binding to Fas receptor), converting an activating APC-to-T cell signal into an inhibitory one. Our previous studies established that CTLA-4·FasL inhibits human primary mixed lymphocyte reactions (MLR) and induces alloantigen-specific hyporesponsiveness ex vivo. The present study extends this to an in vivo context. Using splenocytes from MHC-mismatched C57BL/6 and Balb/c mice, we demonstrated that his6CTLA-4·FasL, effectively inhibits murine MLR. Moving in vivo, we demonstrated that subcutaneously administered his6CTLA-4·FasL modulates the in vivo response of infused allogeneic splenocytes. his6CTLA-4·FasL reduces the number of cells in each cell division, and increases the percentage of dead cells in each division. These findings are consistent with an antigen-induced cell death of the alloreactive cells, and bolsters recombinant TCSP promise as a therapeutic for transplantation diseases." @default.
• W2155322523 created "2016-06-24" @default.
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• W2155322523 date "2006-02-01" @default.
• W2155322523 modified "2023-10-15" @default.
• W2155322523 title "CTLA-4·FasL inhibits allogeneic responses in vivo" @default.
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• W2155322523 doi "https://doi.org/10.1016/j.cellimm.2006.05.002" @default.
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• W2155322523 hasPublicationYear "2006" @default.
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