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炎症小体与自身免疫。

Inflammasomes and autoimmunity.

机构信息

Department of Immunology, St. Jude Children's Research Hospital, MS #351, Suite E7004, 262 Danny Thomas Place, Memphis, TN 38105, USA.

出版信息

Trends Mol Med. 2011 Feb;17(2):57-64. doi: 10.1016/j.molmed.2010.11.001. Epub 2010 Dec 14.

Abstract

The NOD-like receptor (NLR) family members are cytosolic sensors of microbial components and danger signals. A subset of NLRs control inflammasome assembly that results in caspase-1 activation and, in turn, IL-1β and IL-18 production. Excessive inflammasome activation can cause autoinflammatory disorders, including the hereditary periodic fevers. Autoinflammatory and autoimmune diseases form a disease spectrum of aberrant, immune-mediated inflammation against self, through innate and adaptive immunity. However, the role of inflammasomes in autoimmune disease is less clear than in autoinflammation, despite the numerous effects IL-1β and IL-18 can have on shaping adaptive immunity. We summarize the role of inflammasomes in autoimmune disorders, highlight the need for a better understanding of inflammasomes in these conditions and offer suggestions for future research directions.

摘要

NOD 样受体(NLR)家族成员是细胞溶质中微生物成分和危险信号的传感器。NLR 的一个亚群控制着炎性小体的组装,导致半胱氨酸蛋白酶-1 的激活,进而导致白细胞介素-1β 和白细胞介素-18 的产生。过度的炎性小体激活可导致自身炎症性疾病,包括遗传性周期性发热。自身炎症性和自身免疫性疾病形成了一种疾病谱,即先天和适应性免疫对自身的异常、免疫介导的炎症。然而,尽管白细胞介素-1β 和白细胞介素-18 可以对塑造适应性免疫产生众多影响,但炎性小体在自身免疫性疾病中的作用仍不如在自身炎症中那么明确。我们总结了炎性小体在自身免疫性疾病中的作用,强调了需要更好地理解这些疾病中的炎性小体,并为未来的研究方向提供了建议。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41d4/3057120/68c5f67a3a47/nihms259477f1.jpg

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