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作 者:Hongbin Wang Liming Mao Guangxun Meng
机构地区:[1]Unit of Innate Immunity,Key Laboratory of Molecular Virology and Immunology,Institut Pasteur of Shanghai,Shanghai Institutes for Biological Sciences,Chinese Academy of Sciences,Shanghai 200025,China [2]Graduate University of Chinese Academy of Sciences,Beijing 100039,China
出 处:《Protein & Cell》2013年第8期565-568,共4页蛋白质与细胞(英文版)
基 金:This work was supported by grants from 100 Talent Program of the Chinese Academy of Sciences,National Natural Science Foundation of China(Grant Nos.91029707,31170868,812111134,and 31100622);SASIBS Scholarship Program,Chinese Post-doctoral Science Foundation(No.20110490752);Post-doctoral research foundation of Shanghai Institutes for Biological Sciences(No.2011KIP513);the National Science and Technology Key Project(No.2012ZX10002007-003);as well as the CAS/SAFEA International Partnership Program for Creative Research Teams.
摘 要:SIGNAL 1 ALONE IS ENOUGH TO ACTIVATE THE NLRP3 INFLAMMAOSME IN HUMAN CELLS According to our current understanding,the NLR family,pyrin domain containing 3(NLRP3)infl ammasome activation is generally a two-step process.The fi rst step is priming,in which pathogen associated molecular patterns(PAMPs)such as LPS or pro-inflammatory cytokines such as tumor necrosis factor-α(TNF-α)induced NF-κB activation provides synthesis of pro-IL-1βand NLRP3 proteins.This priming step is considered as signal 1,which makes the cell ready for a second strike to assemble the infl ammasome.Then danger signals such as ATP and MSU provide the signal 2 that promotes formation of the NLRP3 infl ammasome and activates caspase-1.Both of these 2 steps are required in mouse macrophages for the NLRP3 inflammasome activation(Dinarello,2007).
关 键 词:NLRP3 ACTIVATION CYTOKINES
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