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首页> 外文期刊>Cytokine >beta2-Adrenergic agonists bias TLR-2 and NOD2 activated dendritic cells towards inducing an IL-17 immune response.
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beta2-Adrenergic agonists bias TLR-2 and NOD2 activated dendritic cells towards inducing an IL-17 immune response.

机译：β2-肾上腺素能激动剂使TLR-2和NOD2激活的树突状细胞偏向诱导IL-17免疫应答。

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This study tested the hypothesis that activation of beta2-adrenoceptors on DCs influences NOD2 signaling along with its cross-talk with Toll-like receptor-2 resulting in altered Th cell priming ability. Th17 cells are a newly discovered lineage of CD4(+) T cells involved in defense against extracellular bacteria and also implicated in autoimmune disorders. Initiation and polarization of the adaptive immune response is controlled by innate immune recognition mediated by DCs. Previous studies demonstrated that adrenergic receptors modulate cytokine production by DCs and affect their Th cell priming ability. We show that the beta2-adrenoceptor agonist salbutamol enhanced IL-6 production in murine bone marrow-derived DCs stimulated with the nucleotide-binding oligomerization domain 2 ligand muramyl dipeptide. However, when the Toll-like receptor-2 ligand Pam3CysSK4 was added, salbutamol inhibited IL-12 but did not alter IL-6 and IL-23 expression. Gene expression analysis showed that salbutamol inhibited the p40 subunit as well as IL-12p35, while IL-23p19 and IL-6 were stimulated. Therefore, beta2-adrenoceptors modulated cytokine production resulting in a Th17 cell priming cytokine pattern. Indeed, when antigen-pulsed DCs stimulated by muramyl dipeptide or Pam3CysSK4+muramyl dipeptide in the presence of salbutamol were used for in vivo immunization, the resulting Th17/Th1 cell ratio was increased as evaluated by IL-17 and IFN-gamma production. In addition, intradermal injection of norepinephrine along with Pam3CysSK4+muramyl dipeptide increased the Th17 response to an immunogenic protein and this effect was reversed by a beta2-adrenoceptor antagonist. Thus, beta2-adrenoceptors may be involved in the regulation of defense against extracellular bacteria and the pathogenesis of inflammatory diseases.
机译：这项研究检验了以下假设：β2-肾上腺素能受体在DC上的激活会影响NOD2信号传导，以及与Toll样受体2的串扰，从而导致Th细胞启动能力改变。 Th17细胞是CD4（+）T细胞的新发现世系，与细胞外细菌防御相关，也与自身免疫性疾病有关。自适应免疫反应的启动和极化受DC介导的先天免疫识别的控制。先前的研究表明，肾上腺素能受体调节DC产生的细胞因子，并影响其Th细胞的启动能力。我们表明，β2肾上腺素受体激动剂沙丁胺醇增强了IL-6的生产，该核苷酸在鼠类骨髓来源的DC中被核苷酸结合的寡聚化域2配体鼠李二肽刺激。但是，当添加Toll样受体2配体Pam3CysSK4时，沙丁胺醇抑制IL-12，但不会改变IL-6和IL-23的表达。基因表达分析表明沙丁胺醇抑制p40亚基以及IL-12p35，同时刺激IL-23p19和IL-6。因此，β2-肾上腺素受体调节细胞因子的产生，导致Th17细胞引发细胞因子的模式。实际上，当在沙丁胺醇存在的情况下使用由嘧啶二肽或Pam3CysSK4 + muramyl二肽刺激的抗原脉冲DC进行体内免疫时，通过IL-17和IFN-γ产生的评估，所得的Th17 / Th1细胞比率增加了。另外，去甲肾上腺素和Pam3CysSK4 + muramyl二肽的皮内注射增加了Th17对免疫原性蛋白质的反应，这种作用被β2-肾上腺素受体拮抗剂逆转。因此，β2-肾上腺素受体可能参与针对细胞外细菌的防御和炎症性疾病的发病机制。

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