Redundant roles for inflammasome receptors NLRP3 and NLRC4 in host defense against Salmonella.

Redundant roles for inflammasome receptors NLRP3 and NLRC4 in host defense against Salmonella.
复制标题

DOI:
10.1084/jem.20100257
复制
发表时间:
2010-08-02
期刊:
The Journal of experimental medicine
影响因子:
--
通讯作者:
Monack DM
Monack DM
中科院分区:
其他
文献类型:
--
作者:
Broz P;Newton K;Lamkanfi M;Mariathasan S;Dixit VM;Monack DM

文献摘要

参考文献

被引文献

相似文献

细胞内病原体和细胞质内的内源性危险信号参与nod样受体(NLRs),它们聚集炎症小体复合物激活caspase-1并促进促炎细胞因子IL-1β和IL-18的释放。然而,体内对微生物病原体有反应的NLRs定义不清。我们发现NLRs NLRP3和NLRC4在鼠伤寒沙门氏菌的反应中都激活了caspase-1。NLRP3和NLRC4响应不同的细菌触发,将ASC和caspase-1募集到单个细胞质焦点,作为pro-IL-1β加工的位点。与NLRP3和NLRC4在先天免疫防御鼠伤寒沙门氏菌中的重要作用一致,缺乏这两种nlr的小鼠明显更容易感染。这些结果揭示了nlr在宿主体内防御细胞内病原体中的意外冗余。
Intracellular pathogens and endogenous danger signals in the cytosol engage NOD-like receptors (NLRs), which assemble inflammasome complexes to activate caspase-1 and promote the release of proinflammatory cytokines IL-1β and IL-18. However, the NLRs that respond to microbial pathogens in vivo are poorly defined. We show that the NLRs NLRP3 and NLRC4 both activate caspase-1 in response to Salmonella typhimurium. Responding to distinct bacterial triggers, NLRP3 and NLRC4 recruited ASC and caspase-1 into a single cytoplasmic focus, which served as the site of pro–IL-1β processing. Consistent with an important role for both NLRP3 and NLRC4 in innate immune defense against S. typhimurium, mice lacking both NLRs were markedly more susceptible to infection. These results reveal unexpected redundancy among NLRs in host defense against intracellular pathogens in vivo.
DOI: 10.4049/jimmunol.0802367
发表时间: 2009-03-01
期刊: Journal of immunology (Baltimore, Md. : 1950)
影响因子: --
作者:
Bryan NB;Dorfleutner A;Rojanasakul Y;Stehlik C
通讯作者: Stehlik C
DOI: 10.1111/j.1462-5822.2008.01177.x
发表时间: 2008-09-01
影响因子: 3.4
作者:
Koo, Ingrid C.;Wang, Chen;Brown, Eric J.
通讯作者: Brown, Eric J.
DOI: 10.1038/ni1346
发表时间: 2006-06-01
期刊: NATURE IMMUNOLOGY
影响因子: 30.5
作者:
Franchi, Luigi;Amer, Amal;Nunez, Gabriel
通讯作者: Nunez, Gabriel
I型干扰素信号在弗朗西斯拉感染过程中激活炎症体需要。
DOI: 10.1084/jem.20062665
发表时间: 2007-05-14
影响因子: 15.3
作者:
Henry, Thomas;Brotcke, Anna;Weiss, David S.;Thompson, Lucinda J.;Monack, Denise M.
通讯作者: Monack, Denise M.
DOI: 10.4049/jimmunol.0901323
发表时间: 2009-09-15
期刊: Journal of immunology (Baltimore, Md. : 1950)
影响因子: --
作者:
Joly S;Ma N;Sadler JJ;Soll DR;Cassel SL;Sutterwala FS
通讯作者: Sutterwala FS