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• W156904150 abstract "Chronic allograft rejection remains the leading cause of death after the first post-transplantation year. The influence of the innate immune system on allograft rejection, particular through toll-likereceptors (TLR) is not fully understood. A pro-inflammatory role in TLR-dependent activation of the immune system is inherited by Trem-1. With the antagonistic synthetic peptide LP17, targeting the extracellular domain of Trem-1, we could demonstrate a prevention of chronic rejection in cardiac allografts. B6.C-H2bm12/KhEg (bm12) donor hearts were transplanted into wild type MHC class II-mismatched C57BL/6J recipient mice. Graft function was assessed by palpation of the abdomen and rejection was defined as cessation of cardiac contractility. For cytokine analysis, CD4+ cells were isolated from donor hearts after transplantation and stimulated with anti-CD3є/CD28. Supernatant was analyzed by ELISA after 48 h. The localization of graft-infiltrating Trem-1+ cells, as well as lymphocyte subsets, was determined with immunohistochemistry and flow cytometry. Upon rejection, starting on day 3, mice were treated daily with antagonistic Trem-1 peptide, LP17 or PBS as control and graft function was defined. Progressive allograft rejection with decreased organ function of bm12-donor hearts was evident starting on day 7–10 and resulted in complete allograft rejection within 4 weeks after transplantation. The accelerated allograft rejection and cellular infiltration is associated with increased production of the proinflammatory cytokines IL-17A and IFN-γ. In addition, the migration of lymphocytes and antigen presenting cells from peripheral blood into donor allografts could be detected. Further analysis of the involvement of the innate immune system in allograft rejection showed a highly increased number of Trem-1+ MHC-class-II+ antigen-presenting cells in the allograft. In contrast, syngenic transplanted hearts completely lack expression of Trem-1+ MHC-class-II+ cells. Furthermore, i. p. administration of LP17 reduced allograft rejection compared to PBS treated mice. Allograft survival in mice treated with LP17 was extended to over 50 days. We could demonstrate the involvement of the innate immune system in chronic allograft rejection. Blocking Trem-1+ antigen-presenting cells resulted in prolongation of allograft survival after cardiac transplantation in mice. Hence, Trem-1 represents a promising target for future therapies for chronic allograft rejection." @default.
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• W156904150 date "2010-01-01" @default.
• W156904150 modified "2023-09-24" @default.
• W156904150 title "Triggering receptor expressed on myeloid cells 1 (Trem-1) als Zielstruktur zur Verlängerung des Transplantatüberlebens bei murinen Herztransplantationen" @default.
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• W156904150 doi "https://doi.org/10.1007/978-3-642-12192-0_61" @default.
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