首页> 外文期刊>European journal of immunology. >Cross‐presentation of dead‐cell‐associated antigens by DNGR‐1+ dendritic cells contributes to chronic allograft rejection in mice
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Cross‐presentation of dead‐cell‐associated antigens by DNGR‐1+ dendritic cells contributes to chronic allograft rejection in mice

机译:交叉作业的死细胞量相关抗原,DNGR 1 +树突细胞的贡献在小鼠慢性同种异体移植物排斥反应

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Abstract The purpose of this study was to elucidate whether DC NK lectin group receptor‐1 (DNGR‐1)‐dependent cross‐presentation of dead‐cell‐associated antigens occurs after transplantation and contributes to CD8+ T?cell responses, chronic allograft rejection (CAR), and fibrosis. BALB/c or C57BL/6 hearts were heterotopically transplanted into WT, Clec9a?/?, or Batf3?/? recipient C57BL/6 mice. Allografts were analyzed for cell infiltration, CD8+ T?cell activation, fibrogenesis, and CAR using immunohistochemistry, Western blot, qRT2‐PCR, and flow cytometry. Allografts displayed infiltration by recipient DNGR‐1+ DCs, signs of CAR, and fibrosis. Allografts in Clec9a?/? recipients showed reduced CAR (p?
机译:摘要本研究之目的阐明是否直流NK凝集素受体组1地理(地理DNGR 1)依赖交叉演示等死细胞相关抗原发生后应承担的移植和有助于CD8 + T ?慢性同种异体移植物排斥反应,(汽车)纤维化heterotopically移植到WT, Clec9a ? / ?还是Batf3 ? / ?分析了细胞渗透,CD8 + T ?激活、纤维发生和汽车使用免疫组织化学、免疫印迹、qRT2检测PCR和流式细胞术。由接收方DNGR高1 + DCs在汽车的迹象,纤维化显示减少汽车(p ? < ?纤维化(p = 0.0001)0.0137), CD8 +细胞浸润(P < 0.0001 ?),和效应细胞因子水平与WT相比收件人。DNGR量1 +直流高渗透在汽车(P < 0.0001 ?),和肝纤维化(P = 0.0382)。同种异体细胞色素C的接受治疗,显示生产CD8效应降低细胞因子(P ? < 0.05)。T ?减少在Clec9a ? / ?0.0283)。受体的基因消除,减少汽车(P = 0.0003),纤维化(P = 0.0273),CD8 +细胞浸润(p = 0.0006)效应细胞因子水平。同种抗原交叉检测演示,DNGR 1 + DCs诱发alloreactive CD8 +细胞诱导的车和纤维化。这个过程,防止汽车和纤维化。

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