Department of Pathology, University of Michigan Medical School Ann Arbor, MI, USA.
Front Immunol. 2013 Jan 9;3:387. doi: 10.3389/fimmu.2012.00387. eCollection 2012.
The complement anaphylatoxin, C5a, through binding to its receptors (C5aR or C5L2), has important biological properties for recruitment and activation of phagocytes. C5a has been identified as a powerful modulator of Toll-like receptor-induced cytokine and chemokine production by macrophages. Both the complement system and the interleukin (IL)-17 cytokine family protect against extracellular pathogens by enhancing innate immune functions. On the basis of its concentration, C5a can either positively or negatively modulate the production by macrophages of IL-17 family members as well as IL-23 via the phosphatidylinositol 3-kinase/Akt signaling cascade. C5a can also affect the production and maintenance of IL-17-producing T cells. Using C5a, C5aR, or C5L2 deficiency or blockade, IL-17/IL-23 production and/or IL-17-dependent disease progression has been shown to be substantially modified. The contributions of C5a interaction with its receptors in the production of IL-17/IL-23 and promotion of IL-17-dependent immune responses are reviewed.
补体过敏毒素 C5a 通过与其受体（C5aR 或 C5L2）结合，对招募和激活吞噬细胞具有重要的生物学特性。C5a 已被确定为巨噬细胞中 Toll 样受体诱导细胞因子和趋化因子产生的有力调节剂。补体系统和白细胞介素（IL）-17 细胞因子家族通过增强先天免疫功能来抵抗细胞外病原体。根据其浓度，C5a 可以通过磷脂酰肌醇 3-激酶/Akt 信号级联正向或负向调节巨噬细胞产生 IL-17 家族成员以及 IL-23 的产生。C5a 还可以影响产生和维持产生 IL-17 的 T 细胞。使用 C5a、C5aR 或 C5L2 缺乏或阻断，已经表明 IL-17/IL-23 的产生和/或 IL-17 依赖性疾病进展会发生实质性改变。本文综述了 C5a 与其受体相互作用在产生 IL-17/IL-23 和促进 IL-17 依赖性免疫反应中的作用。
