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首页> 外文期刊>Clinical and Experimental Immunology: An Official Journal of the British Society for Immunology >Targeted complement inhibition and microvasculature in transplants: a therapeutic perspective
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Targeted complement inhibition and microvasculature in transplants: a therapeutic perspective

机译：靶向补体抑制和微脉管系统在移植中的治疗前景

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Active complement mediators play a key role in graft-versus-host diseases, but little attention has been given to the angiogenic balance and complement modulation during allograft acceptance. The complement cascade releases the powerful proinflammatory mediators C3a and C5a anaphylatoxins, C3b, C5b opsonins and terminal membrane attack complex into tissues, which are deleterious if unchecked. Blocking complement mediators has been considered to be a promising approach in the modern drug discovery plan, and a significant number of therapeutic alternatives have been developed to dampen complement activation and protect host cells. Numerous immune cells, especially macrophages, develop both anaphylatoxin and opsonin receptors on their cell surface and their binding affects the macrophage phenotype and their angiogenic properties. This review discusses the mechanism that complement contributes to angiogenic injury, and the development of future therapeutic targets by antagonizing activated complement mediators to preserve microvasculature in rejecting the transplanted organ.
机译：活性补体介体在移植物抗宿主疾病中起关键作用，但是在同种异体移植接受过程中很少关注血管生成平衡和补体调节。补体级联释放出强大的促炎介质C3a和C5a过敏毒素，C3b，C5b调理素和终末膜攻击复合物进入组织，这些组织如果未经检查就会有害。阻断补体介体已被认为是现代药物发现计划中的一种有前途的方法，并且已经开发出许多治疗性替代品以抑制补体激活并保护宿主细胞。许多免疫细胞，特别是巨噬细胞，会在其细胞表面同时产生过敏毒素和调理素受体，它们的结合会影响巨噬细胞的表型和血管生成特性。这篇综述讨论了补体促成血管生成损伤的机制，以及通过拮抗活化的补体介体以保留排斥移植器官的微脉管系统来发展未来的治疗靶标。

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