The inflammasome NLRs in immunity, inflammation, and associated diseases.

The inflammasome NLRs in immunity, inflammation, and associated diseases.
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DOI:
10.1146/annurev-immunol-031210-101405
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发表时间:
2011
影响因子:
29.7
通讯作者:
Ting JP
Ting JP
中科院分区:
医学1区
文献类型:
--
作者:
Davis BK;Wen H;Ting JP

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炎性小体活化导致半胱天冬酶-1活化,其引起pro-IL-1β和pro-IL-18的成熟裂解。NLR(核苷酸结合域,富含亮氨酸重复序列)蛋白的一个亚组是炎性小体的关键介质。对基因缺陷小鼠和细胞的研究表明,NLR炎性体参与了对多种微生物病原体、炎性疾病、癌症以及代谢和自身免疫性疾病的反应。确定炎性小体在这些疾病和疾病模型中是如何被激活的仍然是一个挑战。本综述介绍并整合了该领域的最新进展。
Inflammasome activation leads to caspase-1 activation, which causes the maturation cleavage of pro-IL-1β and pro-IL-18. A subgroup of the NLR (nucleotide-binding domain, leucine-rich repeat containing) proteins are key mediators of the inflammasome. Studies of gene-deficient mice and cells have implicated NLR inflammasomes in a host of responses to a wide range of microbial pathogens, inflammatory diseases, cancer, and metabolic and autoimmune disorders. Determining exactly how the inflammasome is activated in these diseases and disease models remains a challenge. This review presents and integrates recent progress in the field.
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