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首页> 外文期刊>Cellular Physiology and Biochemistry >Upregulation of Toll-like Receptor (TLR) Expression and Release of Cytokines from Mast Cells by IL-12
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Upregulation of Toll-like Receptor (TLR) Expression and Release of Cytokines from Mast Cells by IL-12

机译：IL-12上调肥大细胞中Toll样受体（TLR）的表达并释放细胞因子

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Background: It has been reported that peptidoglycan (PGN) and lipopolysaccharide (LPS) can provoke mast cells to release an array of cytokines via TLR2 and TLR4, respectively. However, little is known of the regulatory mechanism of TLR2 and TLR4 mediated cytokine production in mast cells. Methods: Since IL-12 plays important roles in protection of the body from microorganism infection and mast cell is a crucial source of IL-12, we investigated effects of IL-12 on expression of TLR2 and TLR4, and cytokine production in mast cells by using quantitative real time PCR, flow cytometry analysis and cellular activation of signaling ELISA techniques. Results: The results showed that IL-12 induced significant increase in expression of TLR2 and TLR4 mRNAs and proteins, respectively. It can also synergistically enhance LPS-induced TLR4 expression in P815 cells. IL-12 not only by itself, but also synergistically enhanced LPS-induced IL-13 release from P815 cells. It appears that IL-12 induced IL-13 release and TLR4 expression is through activation of MAPK and PI3K/Akt signaling pathways, whereas IL-12 induced upregulation of TLR2 is via activation of PI3K/Akt signaling pathway, but not MAPK pathway. Conclusion: The ability of IL-12 in modulation of expression of TLR2 and TLR4 in mast cells, and in stimulation of IL-13 release from mast cells provides further evidence that this cytokine may play a role in the protective immunity against bacteria infection.
机译：背景：据报道，肽聚糖（PGN）和脂多糖（LPS）可以刺激肥大细胞分别通过TLR2和TLR4释放一系列细胞因子。但是，关于肥大细胞中TLR2和TLR4介导的细胞因子产生的调节机制知之甚少。方法：由于IL-12在保护机体免受微生物感染中起着重要作用，而肥大细胞是IL-12的重要来源，因此我们通过以下方法研究了IL-12对TLR2和TLR4表达以及肥大细胞中细胞因子产生的影响。使用实时定量PCR，流式细胞仪分析和信号激活ELISA技术的细胞活化。结果：结果表明IL-12分别诱导TLR2和TLR4 mRNA和蛋白表达显着增加。它也可以协同增强P815细胞中LPS诱导的TLR4表达。 IL-12不仅可以单独发挥作用，而且还可以协同增强LPS诱导的L-13从P815细胞释放。看来IL-12诱导IL-13释放和TLR4表达是通过激活MAPK和PI3K / Akt信号通路，而IL-12诱导TLR2的上调是通过PI3K / Akt信号通路，而不是MAPK通路。结论：IL-12调节肥大细胞中TLR2和TLR4表达的能力以及刺激肥大细胞释放IL-13的能力提供了进一步的证据，表明该细胞因子可能在抵抗细菌感染的保护性免疫中发挥作用。

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