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- W188365280 abstract "Abstract This study evaluated the contribution of the inhibitory molecule B7 homolog-1 (B7-H1) to the regulation of alloimmune responses by pDC. mPDCA-1+ splenic pDC from wild type (WT) or B7-H1 knockout (KO) mice were pulsed with donor antigen (Ag). Cell phenotype was analyzed for Ag-presenting and co-regulatory molecules and T cell allostimulatory capacity was assessed in mixed leukocyte reaction (MLR). WT or KO pDC pulsed with donor Ag were injected into syngeneic mice and CD4+ T cells were purified 7 days later for secondary MLR. T cell proliferation was assessed by 3H-thymidine incorporation and cytokines quantified by ELISA. BALB/c hearts were transplanted into untreated C57BL/6 controls or into mice receiving syngeneic pDC pulsed with donor Ag 7 days before grafting. pDC expressed low levels of CD40, CD80, CD86, MHC I/II, and B7-H1 and showed poor CD4+ T cell stimulatory capacity compared to conventional myeloid DC. pDC from KO mice exhibited greater T cell stimulatory capacity compared to WT controls. T cells from mice given immature, donor Ag-pulsed KO pDC showed greater proliferation and secreted more IFN-γ in secondary MLR compared to WT controls. Recipient-derived, immature WT pDC pulsed with donor Ag prolong allograft survival. These results reveal that B7-H1 on pDC contributes to regulation of alloreactive T cell responses. This work was funded by the transplantation immunology training grant NIAID T32 AI 074490." @default.
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- W188365280 date "2009-04-01" @default.
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- W188365280 title "Host-derived plasmacytoid dendritic cells prolong cardiac allograft survival and regulate alloreactive T cell responses via B7 homolog-1 (141.28)" @default.
- W188365280 doi "https://doi.org/10.4049/jimmunol.182.supp.141.28" @default.
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