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首页> 外文期刊>Infection and immunity >Recombinant human interleukin-2 reverses in vitro-deficient cell-mediated immune responses to tuberculin purified protein derivative by lymphocytes of tuberculous patients.
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Recombinant human interleukin-2 reverses in vitro-deficient cell-mediated immune responses to tuberculin purified protein derivative by lymphocytes of tuberculous patients.

机译:重组人白介素-2逆转结核病患者淋巴细胞对结核菌素纯化蛋白衍生物的体外细胞介导的免疫应答。

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摘要

In vitro lymphocyte proliferative response to purified protein derivative of tuberculin (PPD) was investigated in patients with tuberculosis. Peripheral blood lymphocytes (PBL) from patients with advanced, refractory tuberculosis showed a significantly depressed response compared with the response of PBL from patients with newly diagnosed tuberculosis (P less than 0.01). A further characterization of this low responsiveness to PPD revealed that PBL from these advanced tuberculous patients failed to generate interleukin-2 (IL-2) in response to PPD stimulation. IL-2 receptor (Tac antigen) expression on the surface of T cells after PPD stimulation was also impaired, although to a lesser extent, in the patients with advanced, refractory tuberculosis. We attempted to overcome the depressed in vitro response observed in PBL from patients with advanced, refractory tuberculosis and found that the addition of exogenous, recombinant IL-2 returned the depressed PPD-induced PBL proliferation in these patients to the level of response observed in PBL from patients with newly diagnosed tuberculosis. The addition of recombinant IL-2 also had a restorative effect (up regulation) in vitro on the partly impaired PPD-induced IL-2 receptor expression by PBL from the patients with advanced, refractory tuberculosis. Our results suggest that recombinant IL-2 may offer a novel approach to the therapy of advanced, drug-resistant tuberculosis.
机译:在结核病患者中研究了对结核菌素(PPD)纯化蛋白衍生物的体外淋巴细胞增殖反应。晚期难治性肺结核患者的外周血淋巴细胞(PBL)与新诊断的肺结核患者的PBL反应相比显着降低(P小于0.01)。对PPD的低响应性的进一步特征表明,来自这些晚期结核病患者的PBL无法响应PPD刺激而产生白介素2(IL-2)。 PPD刺激后,T细胞表面的IL-2受体(Tac抗原)表达也受到了损害,尽管程度较轻,但患有晚期难治性结核病患者。我们试图克服晚期,难治性肺结核患者在PBL中观察到的体外应答低下的问题,并发现外源重组IL-2的添加使这些患者中PPD诱导的PBL诱导的PBL增殖降低至PBL中观察到的应答水平来自刚诊断出结核病的患者。重组IL-2的添加在体外对晚期难治性肺结核患者的PBL部分损害了PPD诱导的IL-2受体表达也具有恢复作用(上调)。我们的结果表明,重组IL-2可能为治疗晚期耐药结核病提供一种新颖的方法。

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