A novel "complement-metabolism-inflammasome axis" as a key regulator of immune cell effector function.
A novel "complement-metabolism-inflammasome axis" as a key regulator of immune cell effector function.
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DOI：
10.1002/eji.201546131
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发表时间：
2016-07
影响因子：
5.4
通讯作者：
Kemper, Claudia
中科院分区：
文献类型：
--
作者：
Arbore, Giuseppina;Kemper, Claudia
炎性小体是细胞内多蛋白复合物，其诱导和调节关键促炎细胞因子IL-1β和IL-18的产生以响应感染性微生物和细胞应激。炎性小体的激活涉及几种上游信号，包括经典模式或危险识别系统，如TLR。然而，最近，补体受体（例如过敏毒素C3 a和C5 a受体）和补体调节剂CD 46的活化与细胞代谢变化（例如增加的氨基酸流入和糖酵解（通过mTORC 1））的感测相结合，已经成为炎性小体的另外的关键活化剂。本文综述了我们对补体介导的炎性小体激活的认识的最新进展，特别关注新的“补体-代谢-NLRP 3炎性小体轴”。
The inflammasomes are intracellular multiprotein complexes that induce and regulate the generation of the key pro‐inflammatory cytokines IL‐1β and IL‐18 in response to infectious microbes and cellular stress. The activation of inflammasomes involves several upstream signals including classic pattern or danger recognition systems such as the TLRs. Recently, however, the activation of complement receptors, such as the anaphylatoxin C3a and C5a receptors and the complement regulator CD46, in conjunction with the sensing of cell metabolic changes, for instance increased amino acid influx and glycolysis (via mTORC1), have emerged as additional critical activators of the inflammasome. This review summarizes recent advances in our knowledge about complement‐mediated inflammasome activation, with a specific focus on a novel “complement – metabolism – NLRP3 inflammasome axis.”
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