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研究内皮细胞在实体器官移植中作用的先进研究模型。

Advanced Research Models to Study the Role of Endothelial Cells in Solid Organ Transplantation.

机构信息

Rotterdam Transplant Group, Department of Internal Medicine, Nephrology and Transplantation, Erasmus MC, Erasmus University Medical Center, Rotterdam, Netherlands.

出版信息

Front Immunol. 2021 Feb 10;12:607953. doi: 10.3389/fimmu.2021.607953. eCollection 2021.

Abstract

The endothelium plays a key role in acute and chronic rejection of solid organ transplants. During both processes the endothelium is damaged often with major consequences for organ function. Also, endothelial cells (EC) have antigen-presenting properties and can in this manner initiate and enhance alloreactive immune responses. For decades, knowledge about these roles of EC have been obtained by studying both and models. These experimental models poorly imitate the immune response in patients and might explain why the discovery and development of agents that control EC responses is hampered. In recent years, various innovative human 3D models mimicking organ structure and function have been developed. These models will extend the knowledge about the diverse roles of EC in allograft rejection and will hopefully lead to discoveries of new targets that are involved in the interactions between the donor organ EC and the recipient's immune system. Moreover, these models can be used to gain a better insight in the mode of action of the currently prescribed immunosuppression and will enhance the development of novel therapeutics aiming to reduce allograft rejection and prolong graft survival.

摘要

内皮细胞在实体器官移植的急性和慢性排斥反应中起着关键作用。在这两个过程中,内皮细胞经常受到损伤,这对器官功能有重大影响。此外,内皮细胞(EC)具有抗原呈递特性,因此可以启动和增强同种反应性免疫反应。几十年来,人们通过研究 和 模型来了解 EC 的这些作用。这些实验模型很难模拟患者的免疫反应,这也许可以解释为什么发现和开发控制 EC 反应的药物受到阻碍。近年来,已经开发出各种创新的模拟 器官结构和功能的人类 3D 模型。这些模型将扩展我们对 EC 在同种异体移植排斥反应中的多种作用的认识,并有望发现新的靶点,这些靶点涉及供体器官 EC 与受体免疫系统之间的相互作用。此外,这些模型可用于更深入地了解目前规定的免疫抑制作用的作用模式,并将增强旨在减少同种异体排斥反应和延长移植物存活的新型治疗药物的开发。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c11b/7921837/4681a4270fa5/fimmu-12-607953-g0001.jpg

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