Peng Qi, Li Ke, Sacks Steven H, Zhou Wuding
Complement Laboratory, MRC Centre for Transplantation, King's College London, School of Medicine at Guy's Hospital, London SE1 9RT, UK.
Inflamm Allergy Drug Targets. 2009 Jul;8(3):236-46. doi: 10.2174/187152809788681038.
C3a and C5a, the small (approximately 10KDa) cleavage fragments released by complement activation, are potent mediators of inflammation. They are anaphylatoxins and act as cell activators with nanomolar affinity, exerting their functions through binding to specific receptors (C3aR and C5aR or C5L2 respectively). Recent studies suggest that locally generated complement effector molecules including C3a and C5a contribute to pathological processes in inflammatory and immunological diseases as well as adaptive immune response besides its host defence mechanism. Targeting the receptors and/or their ligands can reduce undesired inflammatory responses and tissue damage in certain pathological conditions. In this article we describe the recent developments in this important area and focus on the role of C3a/C5a in inflammatory and autoimmune diseases and in adaptive immune responses.
C3a和C5a是补体激活释放的小（约10千道尔顿）裂解片段，是炎症的强效介质。它们是过敏毒素，作为具有纳摩尔亲和力的细胞激活剂，通过与特定受体（分别为C3aR和C5aR或C5L2）结合发挥作用。最近的研究表明，包括C3a和C5a在内的局部产生的补体效应分子除了其宿主防御机制外，还参与炎症和免疫疾病的病理过程以及适应性免疫反应。在某些病理条件下，靶向这些受体和/或其配体可以减少不必要的炎症反应和组织损伤。在本文中，我们描述了这一重要领域的最新进展，并重点关注C3a/C5a在炎症和自身免疫性疾病以及适应性免疫反应中的作用。
