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慢性血液透析患者体外白细胞介素-6、肿瘤坏死因子α和白细胞介素-10的产生与临床免疫缺陷相关。

Production of interleukin-6, tumor necrosis factor alpha and interleukin-10 in vitro correlates with the clinical immune defect in chronic hemodialysis patients.

作者信息

Girndt M, Köhler H, Schiedhelm-Weick E, Schlaak J F, Meyer zum Büschenfelde K H, Fleischer B

机构信息

Medical Department IV, University of Homburg/Saar, Germany.

出版信息

Kidney Int. 1995 Feb;47(2):559-65. doi: 10.1038/ki.1995.70.

Abstract

In patients with chronic renal failure alterations in monokine production are a common feature. Their clinical relevance has not yet been proven. We show here a correlation between an overproduction of interleukin-(IL)-6 and tumor necrosis factor alpha (TNF alpha) upon stimulation with LPS by mononuclear cells in vitro and the clinical grade of immunodeficiency found in these patients. Higher levels of IL-6 and TNF alpha were correlated with an immunocompromized state, that is, non-responsiveness to hepatitis B vaccination, whereas patients with a better immune competence showed the same levels of these cytokines as healthy controls. Only the patients with a good immune function showed a high secretion of IL-10. The feedback mechanism of IL-10 for reducing monokine synthesis seems to be intact in these patients. Thus the secretion of IL-10 might be regarded as a compensatory mechanism which controls monokine induction by chronic renal failure and hemodialysis treatment. Immunocompromized patients who are unresponsive to hepatitis B vaccination seem to be unable to enhance IL-10 synthesis for control of monokine overproduction. This results in higher levels of IL-6 and TNF alpha that might be involved in the pathogenesis of reduced immune defense.

摘要

在慢性肾衰竭患者中,单核因子产生的改变是一个常见特征。其临床相关性尚未得到证实。我们在此展示了体外单核细胞经脂多糖刺激后白细胞介素 -6(IL -6)和肿瘤坏死因子α(TNFα)的过度产生与这些患者中发现的免疫缺陷临床分级之间的相关性。IL -6和TNFα的较高水平与免疫受损状态相关,即对乙肝疫苗接种无反应,而免疫能力较好的患者这些细胞因子的水平与健康对照相同。只有免疫功能良好的患者表现出IL -10的高分泌。在这些患者中,IL -10减少单核因子合成的反馈机制似乎是完整的。因此,IL -10的分泌可能被视为一种补偿机制,可控制慢性肾衰竭和血液透析治疗引起的单核因子诱导。对乙肝疫苗接种无反应的免疫受损患者似乎无法增强IL -10合成以控制单核因子的过度产生。这导致IL -6和TNFα水平升高,可能参与免疫防御降低的发病机制。

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