首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Regulation of human B lymphocyte activation by opioid peptide hormones. Inhibition of IgG production by opioid receptor class (mu-, kappa-, and delta-) selective agonists.
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Regulation of human B lymphocyte activation by opioid peptide hormones. Inhibition of IgG production by opioid receptor class (mu-, kappa-, and delta-) selective agonists.

机译:阿片肽激素对人B淋巴细胞活化的调节。阿片受体类别(μ-,κ-和δ-)选择性激动剂对IgG的抑制作用。

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Opioid peptides have been reported by many laboratories to modulate in vitro and in vivo cell-mediated and humoral immune responses. However, less attention has been afforded to the class or classes of opioid receptors involved in these immunomodulatory effects. Previous studies by this laboratory indicated that beta-endorphin and methionine-enkephalin were potent inhibitors of Staphylococcus aureus, Cowen strain I (SAC)-induced IgG production by human B lymphocytes. Results obtained from the present studies indicate that, at pharmacological concentrations, mu-, delta-, and kappa-receptor-selective agonists are potent inhibitors of SAC-induced IgG-secreting cells (IgG-ISC) by human B lymphocytes. Moreover, the suppression of IgG-ISC formation was reversed by mu-, delta-, and kappa-receptor class-selective antagonists, [D'Tic]cTAP, ICI 174,864, and nor-BNI, respectively. These findings are in agreement with other studies showing that more than one class of receptors are involved in opioid peptide-mediated immunoregulation. Additional studies indicated that all three class-selective receptor agonists were found to suppress SAC-induced IL-6 production in intact PBMC cultures. As observed for suppression of IgG-ISC formation, inhibition of IL-6 production was found to be reversed by the appropriate receptor class-selective antagonist. These results support the hypothesis that one mechanism of opioid peptide-mediated inhibition of antibody production is via the down regulation of cytokine synthesis.
机译:阿片肽已经被许多实验室报道,以调节体外和体内细胞介导的和体液免疫应答。然而,对涉及这些免疫调节作用的一种或多种阿片样物质受体的关注较少。该实验室先前的研究表明,β-内啡肽和蛋氨酸-脑啡肽是金黄色葡萄球菌,Cowen株I(SAC)诱导的人B淋巴细胞产生的IgG的有效抑制剂。从本研究中获得的结果表明,在药理学浓度下,μ,δ和κ受体选择性激动剂是人B淋巴细胞SAC诱导的IgG分泌细胞(IgG-ISC)的有效抑制剂。此外,分别由μ-,δ-和κ受体类选择性拮抗剂[D'Tic] cTAP,ICI 174,864和nor-BNI逆转了IgG-ISC形成的抑制作用。这些发现与其他研究一致,后者表明阿片肽介导的免疫调节涉及一种以上的受体。进一步的研究表明,在完整的PBMC培养物中,发现所有三种类别选择性受体激动剂均能抑制SAC诱导的IL-6产生。如对IgG-ISC形成的抑制所观察到的,发现IL-6产生的抑制被适当的受体类别选择性拮抗剂逆转。这些结果支持以下假设:阿片肽介导的抗体产生抑制的一种机制是通过下调细胞因子合成。

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