Production of tumor necrosis factor-alpha and interferon-gamma from human peripheral blood lymphocytes by MGN-3, a modified arabinoxylan from rice bran, and its synergy with interleukin-2 in vitro.
Production of tumor necrosis factor-alpha and interferon-gamma from human peripheral blood lymphocytes by MGN-3, a modified arabinoxylan from rice bran, and its synergy with interleukin-2 in vitro.
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发表时间：
2000
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通讯作者：
M. Ghoneum;A. Jewett
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作者：
M. Ghoneum;A. Jewett
最近，我们提出了从米糠中提取的酶修饰阿拉伯木聚糖MGN-3在体内和体外有效激活人类自然杀伤（NK）细胞功能中的作用的证据。在目前的研究中，我们研究了MGN-3提高NK细胞毒活性的机制。我们通过测试MGN-3对肿瘤坏死因子- α (tnf - α)和干扰素- γ (ifn - γ)分泌水平的作用以及MGN-3对关键细胞表面受体表达的功能来做到这一点。用浓度分别为0.1 mg/ml和1 mg/ml的MGN-3处理外周血淋巴细胞，上清液进行酶联免疫吸附试验。结果表明，MGN-3是一种有效的tnf - α诱导剂。这种效果是剂量依赖性的。MGN-3浓度为0.1和1mg /ml时，tnf - α的产生分别增加22.8%和47%。分别1-fold。MGN-3也增加了ifn - γ的产生，但与tnf - α相比，其水平较低。对于关键的细胞表面受体，MGN-3在治疗后16小时增加了CD69的表达，CD69是一种早期活化抗原。此外，MGN-3处理后，白细胞介素-2受体CD25和粘附分子ICAM-1 （CD54）上调。用MGN-3处理高度纯化的NK细胞也导致tnf - α和ifn - γ分泌水平增加，同时增强NK细胞的细胞毒性功能。此外，在白细胞介素-2活化的NK细胞中添加MGN-3导致tnf - α和ifn - γ分泌的协同诱导。总的来说，我们的数据表明，MGN-3作为一种新的生物反应调节剂，可以作为现有免疫治疗方式的安全替代品或辅助剂。
Recently, we presented evidence for the role of MGN-3, an enzymatically modified arabinoxylan extracted from rice bran, in potent activation of human natural killer (NK) cell function in vivo and in vitro. In the current study, we examined the mechanism by which MGN-3 elevated NK cytotoxic activity. We did this by testing the action of MGN-3 on the levels of both tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) secretions and MGN-3 function on the expression of key cell surface receptors. Peripheral blood lymphocytes were treated with MGN-3 at concentrations of 0.1 mg/ml and 1 mg/ml, and supernatants were subjected to enzyme-linked immunosorbent assay. Results showed that MGN-3 is a potent TNF-alpha inducer. The effect was dose-dependent. MGN-3 concentration at 0.1 and 1 mg/ml increased TNF-alpha production by 22.8- and 47. 1-fold, respectively. MGN-3 also increased production of IFN-gamma but at lower levels as compared to TNF-alpha With respect to key cell surface receptors, MGN-3 increases the expression of CD69, an early activation antigen at 16 hours after treatment. Furthermore, the interleukin-2 receptor CD25 and the adhesion molecule ICAM-1 (CD54) were upregulated after treatment with MGN-3. Treating highly purified NK cells with MGN-3 also resulted in increased levels of TNF-alpha and IFN-gamma secretion in conjunction with augmentation of NK cell cytotoxic function. Furthermore, addition of MGN-3 to interleukin-2-activated NK cells resulted in a synergistic induction of TNF-alpha and IFN-gamma secretion. Overall, our data suggest that MGN-3, a novel biological response modifier, can be used as a safe alternative or as an adjuvant to the existing immunotherapeutic modalities.