Involvement of interleukin-1 receptor-associated kinase (IRAK)-M in toll-like receptor (TLR) 7-mediated tolerance in RAW 264.7 macrophage-like cells
Involvement of interleukin-1 receptor-associated kinase (IRAK)-M in toll-like receptor (TLR) 7-mediated tolerance in RAW 264.7 macrophage-like cells
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DOI：
10.1016/j.cellimm.2009.01.013
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发表时间：
2009-01-01
影响因子：
4.3
通讯作者：
Yokochi, Takashi
中科院分区：
文献类型：
--
作者：
Hassan, Ferdaus;Islam, Shamima;Yokochi, Takashi
为了建立新的TLR介导的耐受性，检查了Toll样受体（TLR）7配体预处理对响应于TLR 7或TLR 2配体的肿瘤坏死因子（TNF）-α的产生的影响。用咪喹莫特R837作为TLR 7配体处理RAW 264.7巨噬细胞样细胞18小时，洗涤并在新鲜培养基中孵育6小时。用咪喹莫特R837作为TLR 7配体或Pam 3CysSK 4作为TLR 2配体的第二次攻击导致TLR 7配体预处理的细胞中TNF-α产生减少。在耐受细胞中存在NF-κ B B、p38和应激活化蛋白激酶（SAPK）的活化受损。IRAK-M作为TLR信号的负调控因子在耐受细胞中的表达显著增强，而白细胞介素-1受体相关激酶（IRAK）-1功能正常。IRAK-M参与TLR 7介导的耐受性进行了讨论。(C)2009 Elsevier Inc. All rights reserved.
The effect of toll-like receptor (TLR) 7 ligand pretreatment on the production of tumor necrosis factor (TNF)-alpha in response to TLR7 or TLR2 ligand was examined in order to establish a new TLR-mediated tolerance. RAW 264.7 macrophage-like cells were treated with imiquimod R837 as a TLR7 ligand for 18 h, washed and incubated in fresh culture medium 6 h. The second challenge with imiquimod R837 as a TLR7 ligand or Pam3CysSK4 as a TLR2 ligand resulted in reduced TNF-alpha production in TLR7 ligand-pretreated cells. There was impaired activation of NF-kappa B, p38 and stress-activated protein kinase (SAPK) in the tolerant cells. The expression of IRAK-M as a negative regulator of TLR signaling was markedly augmented in the tolerant cells while the interlelikin-1 receptor-associated kinase (IRAK)-1 functioned normally. The involvement of IRAK-M in the TLR7-mediated tolerance is discussed. (C) 2009 Elsevier Inc. All rights reserved.