Numerous diseases are driven by chronic inflammation, placing major burdens on our health systems. Controlling inflammation is an important preventative and therapeutic goal. Over 40 “Complement” proteins are produced in blood or on cell surfaces through activation of the Complement protein network mainly by infection or injury. These proteins complement immune cells and antibodies to identify, tag, destroy, and eliminate pathogens and infected or damaged cells and repair tissues. If the inflammatory stimulus is not removed by localized acute immune responses, Complement activation may be prolonged or misdirected to healthy cells, and chronic inflammation can lead to inflammatory or autoimmune diseases. The formation, structures, and interplay between Complement proteins are complex, and this has limited our detailed understanding of their roles and importance in physiology and disease. With the availability of new structures for Complement proteins, new knowledge of how they function, and new modulators of Complement-driven signaling, there are also new opportunities to intervene in Complement-mediated disease. Small molecule and peptide-based drug leads, identified as clues for Complement-directed therapeutic development, are assembled here together with the available evidence for their efficacy in cellular and animal models of human inflammatory disease and in some human clinical conditions.

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调节补体介导疾病的化学方法

许多疾病是由慢性炎症驱动的，这给我们的卫生系统带来了沉重负担。控制炎症是重要的预防和治疗目标。血液或细胞表面通过主要通过感染或损伤激活补体蛋白网络而产生40多种“补体”蛋白。这些蛋白质补充免疫细胞和抗体，以识别，标记，破坏和消除病原体，感染或受损的细胞并修复组织。如果不能通过局部急性免疫反应消除炎症刺激，补体激活可能会延长或误导至健康细胞，并且慢性炎症会导致炎症或自身免疫性疾病。补体蛋白之间的形成，结构和相互作用是复杂的，这限制了我们对它们在生理和疾病中的作用和重要性的详细了解。随着补体蛋白新结构的出现，其功能的新知识以及补体驱动信号转导的新调节剂的介入，也有新的机会介入补体介导的疾病。小分子和肽基药物线索被确定为补体定向治疗发展的线索，在这里与它们在人类炎性疾病的细胞和动物模型以及某些人类临床状况下的有效性的可用证据一起组装。也有新的机会来干预补体介导的疾病。小分子和肽基药物线索被确定为补体定向治疗发展的线索，在这里与它们在人类炎性疾病的细胞和动物模型以及某些人类临床状况下的有效性的可用证据一起组装。也有新的机会来干预补体介导的疾病。小分子和肽基药物线索被确定为补体定向治疗发展的线索，在这里与它们在人类炎性疾病的细胞和动物模型以及某些人类临床状况下的有效性的可用证据一起组装。