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首页> 外文期刊>Life sciences >Critical roles of acetylcholine and the muscarinic and nicotinic acetylcholine receptors in the regulation of immune function.
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Critical roles of acetylcholine and the muscarinic and nicotinic acetylcholine receptors in the regulation of immune function.

机译：乙酰胆碱和毒蕈碱和烟碱乙酰胆碱受体在免疫功能调节中的关键作用。

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Lymphocytes express both muscarinic and nicotinic acetylcholine (ACh) receptors (mAChRs and nAChRs, respectively), and stimulation of mAChRs and nAChRs produces various biochemical and functional changes. Although it has been postulated that parasympathetic cholinergic nerves directly innervate immune cells, no evidence has supported this hypothesis. We measured ACh in the blood of various animal species and determined its localization in T cells using a sensitive and specific radioimmunoassay. Furthermore, we showed that T cells express choline acetyltransferase (ChAT), an ACh synthesizing enzyme. Immunological T cell activation enhances ACh synthesis through the up-regulation of ChAT expression, suggesting lymphocytic cholinergic activity is related to immunological activity. Most immune cells such as T cells, B cells, and monocytes express all five subtypes of mAChRs (M(1)-M(5)), and various subunits of the nAChR, such as α3, α5, α7, α9, and α10. Studies on serum antibody production in M(1) and M(5) combined mAChR gene knockout (KO) mice immunized with ovalbumin (OVA) revealed that M(1)/M(5) mAChRs up-regulate TNF-α, IFN-γ and IL-6 production in spleen cells, leading to an elevation of serum anti-OVA specific IgG(1). In contrast, studies of nAChR α7 subunit gene KO mice immunized with OVA show that α7 nAChRs down-regulate these proinflammatory cytokines, thereby leading to a reduction of anti-OVA specific IgG(1). Taken together, these findings demonstrate that both mAChRs and nAChRs modulate production of cytokines, such as TNF-α, resulting in a modification of antibody production. These findings support the notion that a non-neuronal cholinergic system is involved in the regulation of immune cell function.
机译：淋巴细胞表达毒蕈碱和烟碱乙酰胆碱（ACH）受体（SHARRS和NACHR），并且MACHR和NACHRS的刺激产生各种生物化学和功能变化。虽然已经假定了副交感神经胆碱能神经直接关联免疫细胞，但没有证据支持这一假设。我们测量了各种动物物种的血液中的ACH，并使用敏感和特异的放射免疫测定法测定其在T细胞中的定位。此外，我们表明T细胞表达胆碱乙酰转移酶（聊天），一种ACH合成酶。免疫学T细胞活化通过聊天表达的上调增强ACH合成，表明淋巴细胞胆碱能活性与免疫活性有关。大多数免疫细胞如T细胞，B细胞和单核细胞表达了所有五种Machr（m（1）-m（5））的亚型，以及NACHR的各种亚基，例如α3，α5，α7，α9和α10 。用卵烧蛋（OVA）免疫的M（1）和M（5）组合MachR基因敲除（KO）小鼠的血清抗体产生的研究显示，M（1）/ m（5）MACHR上调TNF-α，IFN-液体细胞中γ和IL-6产生，导致血清抗卵子特异性IgG（1）的升高。相反，用卵子免疫的NACHRα7亚基基因KO小鼠的研究表明，α7nAChrs下调这些促炎细胞因子，从而降低了抗-OVA特异性IgG（1）的降低。这些研究结果一起表明，MACHR和NACHRS调节细胞因子的产生，例如TNF-α，导致抗体产生的改性。这些发现支持非神经元胆碱能系统参与免疫细胞功能调节的观念。

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