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RCC 与同种异体肾移植排斥中的免疫机制。

Immunologic mechanisms in RCC and allogeneic renal transplant rejection.

机构信息

Department of Urology, Eberhard Karls University Tübingen, 72076 Tübingen, Germany.

出版信息

Nat Rev Urol. 2010 Jun;7(6):339-47. doi: 10.1038/nrurol.2010.59. Epub 2010 May 11.

DOI:10.1038/nrurol.2010.59
PMID:20458329
Abstract

The tolerance state that exists between renal cell carcinoma (RCC) and the host's immune system would be an ideal situation in the setting of human kidney transplantation, in which graft tolerance is the ultimate goal of immunosuppressive therapy. On the other hand, acute rejection, as it appears in renal allografts, would be the optimal immunologic situation in patients with RCC. Analysis of the underlying mechanisms of acute allograft rejection and local pro-tumor immunosuppression could help to identify potential therapeutic targets for inducing immune tolerance in allograft recipients and immune rejection in RCC patients. Experimental kidney transplantation might be a suitable model in which to analyze these processes. Macrophages are a prominent and vital cell type in the cellular infiltrate seen in both RCC and renal allografts. Depending on their polarization, they can initiate and promote either proinflammatory or pro-tumor responses, which lead to tissue rejection or acceptance, respectively. Improved understanding of macrophage biology could lead to therapeutic modification of their function in order to promote a desirable immunologic response in either RCC or transplant tissue.

摘要

在人类肾移植中,存在于肾细胞癌 (RCC) 和宿主免疫系统之间的耐受状态将是一种理想的情况,其中移植物耐受是免疫抑制治疗的最终目标。另一方面,急性排斥反应,如其在肾移植中的表现,将是 RCC 患者的最佳免疫状态。分析急性同种异体移植物排斥反应和局部抗肿瘤免疫抑制的潜在机制,可以帮助确定诱导移植受者免疫耐受和 RCC 患者免疫排斥的潜在治疗靶点。实验性肾移植可能是分析这些过程的合适模型。巨噬细胞是 RCC 和肾移植中细胞浸润的突出和重要细胞类型。根据它们的极化状态,它们可以引发和促进促炎或抗肿瘤反应,分别导致组织排斥或接受。更好地了解巨噬细胞生物学可以导致对其功能进行治疗性修饰,以促进 RCC 或移植组织中理想的免疫反应。

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A novel CXCL8 protein-based antagonist in acute experimental renal allograft damage.一种新型 CXCL8 蛋白为基础的拮抗剂在急性实验性肾移植损伤中的作用。
Mol Immunol. 2010 Feb;47(5):1047-57. doi: 10.1016/j.molimm.2009.11.012. Epub 2009 Dec 11.
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