首页> 美国卫生研究院文献>Annals of the Rheumatic Diseases >Phytohaemagglutinin induced proliferation of lymphocytes from patients with rheumatoid arthritis and iron deficiency.
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Phytohaemagglutinin induced proliferation of lymphocytes from patients with rheumatoid arthritis and iron deficiency.

机译:植物血凝素诱导类风湿性关节炎和铁缺乏症患者淋巴细胞的增殖。

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摘要

The response of peripheral blood lymphocytes to stimulation by mitogens such as phytohaemagglutinin (PHA) is commonly depressed in both rheumatoid arthritis and iron deficiency, and as many rheumatoid patients are anaemic with evidence of abnormal iron metabolism it is possible that the same mechanism underlies the observed suppression in both conditions. In the present study the mitogenic response to PHA of lymphocytes from three rheumatoid patients, who were also iron deficient, and two healthy controls has been shown to be significantly less in iron deficient than iron containing media (p less than 0.001). In addition, iron deficient sera from these patients reduced the PHA induced proliferation of lymphocytes from a normal subject (p less than 0.01), an effect which was prevented by prior addition of iron to these serum samples. In iron containing media lymphocytes from five patients and two controls showed no difference in their response to PHA for both the minimum mitogen concentration which enhanced transformation and the peak [3H]thymidine uptake; but patients' lymphocytes showed significantly less response to PHA concentrations of 5 and 10 mg/l (p less than 0.02), resulting in a reduction in the area under the dose response curves up to 20 mg/l (p less than 0.05). These findings show both that iron deficient sera can impair PHA induced lymphocyte transformation and that lymphocytes from iron deficient rheumatoid patients have impaired responsiveness to PHA. Iron is known to be required intracellularly for the enzyme ribonucleotide reductase, which is important for DNA synthesis, and reduced activity of this enzyme could explain these observed effects.
机译:在类风湿关节炎和铁缺乏症中,外周血淋巴细胞对有丝分裂原(例如植物血凝素(PHA))刺激的反应通常会受到抑制,并且由于许多类风湿病患者贫血且铁代谢异常的证据,有可能是观察到相同机制的基础在两种情况下都受到抑制。在本研究中,三名类风湿病患者的淋巴细胞对PHA的促有丝分裂反应也都是铁缺乏症,而两个健康对照组的铁缺乏症明显低于含铁培养基(p小于0.001)。此外,这些患者的铁缺乏血清减少了正常人PHA诱导的淋巴细胞增殖(p小于0.01),这种作用可通过事先向这些血清样品中添加铁来防止。在含铁培养基中,来自五名患者和两个对照组的淋巴细胞对促转化的最小促分裂原浓度和[3H]胸苷摄取峰值均无反应。但是患者的淋巴细胞对PHA浓度为5和10 mg / l的反应明显较少(p小于0.02),导致剂量反应曲线下的面积减少了20 mg / l(p小于0.05)。这些发现表明铁缺乏血清可以损害PHA诱导的淋巴细胞转化,铁缺乏类风湿患者的淋巴细胞也损害了对PHA的反应性。已知铁是核糖核苷酸还原酶在细胞内所必需的,这对DNA合成很重要,该酶活性降低可以解释这些观察到的作用。

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