调节NLRP3炎性小体激活的分子机制。
Molecular mechanisms regulating NLRP3 inflammasome activation.
作者信息
Jo Eun-Kyeong, Kim Jin Kyung, Shin Dong-Min, Sasakawa Chihiro
机构信息
Department of Microbiology, Chungnam National University School of Medicine, Daejeon 301-747, South Korea.
Infection Signaling Network Research Center, Chungnam National University School of Medicine, Daejeon 301-747, South Korea.
出版信息
Cell Mol Immunol. 2016 Mar;13(2):148-59. doi: 10.1038/cmi.2015.95. Epub 2015 Nov 9.
Abstract
Inflammasomes are multi-protein signaling complexes that trigger the activation of inflammatory caspases and the maturation of interleukin-1β. Among various inflammasome complexes, the NLRP3 inflammasome is best characterized and has been linked with various human autoinflammatory and autoimmune diseases. Thus, the NLRP3 inflammasome may be a promising target for anti-inflammatory therapies. In this review, we summarize the current understanding of the mechanisms by which the NLRP3 inflammasome is activated in the cytosol. We also describe the binding partners of NLRP3 inflammasome complexes activating or inhibiting the inflammasome assembly. Our knowledge of the mechanisms regulating NLRP3 inflammasome signaling and how these influence inflammatory responses offers further insight into potential therapeutic strategies to treat inflammatory diseases associated with dysregulation of the NLRP3 inflammasome.
摘要
炎性小体是触发炎性半胱天冬酶激活和白细胞介素-1β成熟的多蛋白信号复合物。在各种炎性小体复合物中，NLRP3炎性小体的特征最为明确，并且与多种人类自身炎症性和自身免疫性疾病有关。因此，NLRP3炎性小体可能是抗炎治疗的一个有前景的靶点。在这篇综述中，我们总结了目前对NLRP3炎性小体在细胞质中被激活的机制的理解。我们还描述了激活或抑制炎性小体组装的NLRP3炎性小体复合物的结合伙伴。我们对调节NLRP3炎性小体信号传导的机制以及这些机制如何影响炎症反应的了解，为治疗与NLRP3炎性小体失调相关的炎症性疾病的潜在治疗策略提供了进一步的见解。
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