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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Langerhans cells beta2-adrenoceptors: role in migration, cytokine production, Th priming and contact hypersensitivity.
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Langerhans cells beta2-adrenoceptors: role in migration, cytokine production, Th priming and contact hypersensitivity.

机译：Langerhans细胞beta2-肾上腺素受体：在迁移，细胞因子产生，Th启动和接触超敏反应中起作用。

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We showed that norepinephrine (NE) hampers IL-12 and stimulates IL-10 production via adrenoceptors (ARs) in bone marrow-derived dendritic cells (BMDC) influencing their Th priming ability. Others have shown that Langerhans cells (LC) express mRNA for beta1-, beta2- and alpha1(A)-(ARs) and that catecholamines may inhibit the antigen-presenting capability via beta2-ARs. Here, we show that also BMDC express mRNA for beta1-, beta2-, alpha2(A)- and alpha2(C)-ARs. Inhibition of IL-12 is mediated by both beta2- and alpha2(A)-ARs, while stimulation of IL-10 by beta2-ARs only. In addition, LC migration, the contact hypersensitivity response (CHS) and production of IFN-gamma and IL-2 in draining lymph node cells is increased in mice treated topically with the beta2-AR antagonist ICI 118,551 during FITC sensitization. Activation of beta2-ARs in BMDC before adoptive transfer could reduce both migration and CHS response to FITC. Finally, preincubation of BMDC with LPS in presence of the specific beta2-AR agonist salbutamol impaired their chemotactic response to CCL19 and CCL21 and this effect was neutralized by anti-IL-10 mAb. We suggest that the physiological activation of beta2-ARs in DC (LC) results in stimulation of IL-10 which in turn restrains DC (LC) migration influencing antigen presentation and the consequent CHS response.
机译：我们显示，去甲肾上腺素（NE）会阻碍IL-12并通过骨髓衍生树突状细胞（BMDC）中的肾上腺素能受体（ARs）刺激IL-10的产生，从而影响其Th启动能力。其他研究表明，朗格汉斯细胞（LC）表达针对beta1，beta2-和alpha1（A）-（ARs）的mRNA，而儿茶酚胺可能通过beta2-ARs抑制抗原呈递能力。在这里，我们表明BMDC也表达beta1，beta2，alpha2（A）-和alpha2（C）-ARs的mRNA。 IL-12的抑制作用是由beta2-和alpha2（A）-ARs介导的，而仅由beta2-ARs刺激IL-10。此外，在FITC致敏期间，局部用β2-AR拮抗剂ICI 118,551治疗的小鼠的LC迁移，接触性超敏反应（CHS）以及引流淋巴结细胞中IFN-γ和IL-2的产生均增加。在过继转移之前激活BMDC中的beta2-ARs可以减少迁移和CHS对FITC的反应。最后，在存在特定的β2-AR激动剂沙丁胺醇的情况下，用LPS对BMDC进行预温育会削弱其对CCL19和CCL21的趋化反应，并且该作用会被抗IL-10 mAb中和。我们建议，在DC（LC）中β2-ARs的生理活化导致IL-10的刺激，进而刺激IL-10迁移，从而影响抗原呈递和随后的CHS反应。

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