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首页> 外文期刊>Cellular immunology >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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Involvement of interleukin-1 receptor-associated kinase (IRAK)-M in toll-like receptor (TLR) 7-mediated tolerance in RAW 264.7 macrophage-like cells.

机译：白介素-1受体相关激酶（IRAK）-M参与RAW 264.7巨噬细胞样细胞中的toll样受体（TLR）7介导的耐受性。

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摘要

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 18h, washed and incubated in fresh culture medium 6h. 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-kappaB, 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 interleukin-1 receptor-associated kinase (IRAK)-1 functioned normally. The involvement of IRAK-M in the TLR7-mediated tolerance is discussed.
机译：为了建立新的TLR介导的耐受性，研究了Toll样受体（TLR）7配体预处理对响应TLR7或TLR2配体的肿瘤坏死因子（TNF）-α产生的影响。用咪喹莫特R837作为TLR7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。以咪喹莫特R837作为TLR7配体或以Pam3CysSK4作为TLR2配体的第二个挑战导致经TLR7配体预处理的细胞中TNF-α产量降低。耐受细胞中NF-κB，p38和应激激活蛋白激酶（SAPK）的激活受损。 IRAK-M作为TLR信号的负调节剂的表达在耐受细胞中显着增加，而白介素1受体相关激酶（IRAK）-1正常发挥作用。讨论了IRAK-M与TLR7介导的耐受性的关系。

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