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皮质类固醇疗法可抑制活动性肺结节病患者肺T淋巴细胞的自发性白细胞介素2释放和自发性增殖。

Corticosteroid therapy suppresses spontaneous interleukin 2 release and spontaneous proliferation of lung T lymphocytes of patients with active pulmonary sarcoidosis.

作者信息

Pinkston P, Saltini C, Müller-Quernheim J, Crystal R G

出版信息

J Immunol. 1987 Aug 1;139(3):755-60.

PMID:3496388
Abstract

Active pulmonary sarcoidosis is characterized by the alveolar accumulation of activated helper T lymphocytes that are spontaneously releasing IL 2 and proliferating at an enhanced rate. In this regard, sarcoidosis represents a "model" human disorder to test in vivo the known in vitro action of corticosteroids on suppressing the activated IL 2 gene. Comparable groups of patients with active sarcoidosis were prospectively evaluated with no therapy or treated with corticosteroids. Over 3.2 +/- 0.4 mo, the untreated group had no significant change in spontaneous lung T cell release of IL 2 or spontaneous proliferation. In contrast, over the same period, the treated group had marked reduction of spontaneous lung T cell release of IL 2 and proliferation (p less than 0.01, all comparisons before therapy). Furthermore, Northern analysis of lung T cell RNA before therapy demonstrated IL 2 mRNA transcripts, whereas no IL 2 transcripts were observed during therapy. These observations are consistent with the concept that directly, or indirectly, corticosteroids are capable of suppressing the IL 2 gene in activated T lymphocytes in vivo.

摘要

活动性肺结节病的特征是活化的辅助性T淋巴细胞在肺泡内积聚,这些细胞会自发释放白细胞介素2(IL 2)并以更快的速度增殖。在这方面,结节病是一种“模型”人类疾病,可用于在体内测试皮质类固醇对抑制活化的IL 2基因的已知体外作用。对可比的活动性结节病患者组进行前瞻性评估,一组不接受治疗,另一组接受皮质类固醇治疗。在3.2±0.4个月的时间里,未治疗组的肺T细胞自发释放IL 2或自发增殖没有显著变化。相比之下,在同一时期,治疗组的肺T细胞自发释放IL 2和增殖明显减少(所有治疗前比较,p<0.01)。此外,治疗前对肺T细胞RNA进行的Northern分析显示有IL 2 mRNA转录本,而在治疗期间未观察到IL 2转录本。这些观察结果与以下概念一致,即皮质类固醇能够直接或间接在体内抑制活化T淋巴细胞中的IL 2基因。

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