两例结节病患者建立的对自体外周血单核细胞应答的1型辅助T细胞系。

Sarcoidosis Pub Date : 1995-09-01
K Kawakami, I Owan, H Kaneshima, A Saito
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引用次数: 0

摘要

在本研究中,分别从活动性结节病患者的支气管肺泡灌洗液(BAL)和受影响的淋巴结中通过IL-2培养建立T细胞系TU/BAL和KC/LN。这些细胞系产生IL-2,并通过丝裂霉素C处理的患者自身外周血单核细胞的刺激增殖,而其他三种由cona刺激的非结节性肺疾病患者BAL细胞建立的T细胞系没有表现出任何增殖反应。IL-2介导了细胞的增殖,因为抗il - 2r α链单克隆抗体(mAb)以剂量依赖的方式抑制了这种反应。贴壁细胞是细胞增殖的主要刺激物。CD4和HLA-DR似乎都参与其中,因为针对这些分子的单克隆抗体抑制了这种反应。这些结果表明,从肉瘤患者获得的T细胞对某种与HLA-DR相关的未知抗原或在单核细胞上表达的某些自身抗原有反应。此外,TU/BAL和KN/LN都代表了th1样细胞的特征:在存在或不存在12- o -十四烷醇-13-醋酸酯的情况下,当受到PHA刺激时,它们分泌IL-2和ifn - γ,但不分泌IL-4、IL-5和IL-6。因此,被某些未知抗原激活的th1样细胞可能在结节病的发病机制中起作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Type 1-like helper T cell lines responsive to autologous peripheral blood monocytes established from two patients with sarcoidosis.

In the present study, T cell lines, designated TU/BAL and KC/LN, were established from bronchoalveolar lavage (BAL) fluid and an affected lymph node, respectively, obtained from patients with active sarcoidosis by cultivating in the presence of IL-2. These cell lines produced IL-2 and proliferated by stimulation with the patient's own peripheral blood mononuclear cells treated with mitomycin C, while three other T cell lines established from ConA-stimulated BAL cells of patients with non-sarcoid lung diseases did not show any proliferative responses. The proliferation was mediated by IL-2, because anti-IL-2R alpha-chain monoclonal antibody (mAb) inhibited this response in a dose-dependent fashion. The adherent cell was a main stimulator of the proliferation. Both CD4 and HLA-DR appeared to be involved, because mAbs against these molecules inhibited this response. These results suggest that T cells obtained from sarcoid patients respond to a certain unknown antigen associated with HLA-DR or some self antigen expressed on the monocytes. Furthermore, both TU/BAL and KN/LN represented a profile of Th1-like cells: they secreted IL-2 and IFN-gamma, but not IL-4, IL-5 and IL-6, when stimulated with PHA in the presence or absence of 12-O-tetradecanoylphorbol-13-acetate. Thus, Th1-like cells activated by some unknown antigen(s) might play roles in the pathogenesis of sarcoidosis.

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