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- W4313355962 abstract "Abstract The long-term success of lung transplantation is mainly limited by the development of obliterative bronchiolitis (OB) in which IL-17 plays a critical role. However, murine orthotopic allogeneic lung transplant model in wild type recipients develops IFNγ-dominant acute allograft rejection. Our previous research demonstrated that additional STAT6 deficiency to T-bet deficiency resulted in Th17-dominant immune responses, and also restored CD4 T cells to produce IFNγ which is essential to immunosuppression and immunological tolerance. In this study, murine orthotopic lung transplants were performed in C57BL/6 wild type or T-bet/STAT6 double knout-out (DKO) mice using BALB/c donors. Vigorous allograft rejection was observed in T-bet/STAT6 DKO recipients with much higher levels of IL-17 but comparable levels of IFNγ expression to that in wild type recipients. Analysis of the graft-infiltrating cells displayed a significantly decreased CD4:CD8 ratio in T-bet/STAT6 DKO recipients compared to wild type recipients, but not as extremely as that observed in T-bet KO recipients, demonstrating more balanced CD4 and CD8 responses in DKO recipients. Our results indicate T-bet and STAT6 double deficient recipients of lung allografts develop obliterative airway inflammation that is mediated by both CD4 and CD8 responses, more closely resembling OB pathogenesis, and provide a new viable model to study lung transplant rejection." @default.
- W4313355962 created "2023-01-06" @default.
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- W4313355962 date "2017-05-01" @default.
- W4313355962 modified "2023-09-26" @default.
- W4313355962 title "STAT6 and T-bet double deficient mouse serving as allograft recipient is a new viable animal model to study lung transplantation" @default.
- W4313355962 doi "https://doi.org/10.4049/jimmunol.198.supp.82.25" @default.
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