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环孢素A对克隆化T细胞的免疫抑制作用。

Immunosuppressive effects of cyclosporin A on cloned T cells.

作者信息

Herold K C, Lancki D W, Moldwin R L, Fitch F W

出版信息

J Immunol. 1986 Feb 15;136(4):1315-21.

PMID:2935576
Abstract

The effects of the immunosuppressive agent Cyclosporin A (CsA) on the immune response of T lymphocytes are not clearly understood. Much of the previous data are conflicting, possibly due to the study of bulk populations of cells. Therefore, we studied the effects of CsA on cloned murine helper T lymphocytes (HTL) and cytolytic T lymphocytes (CTL) after stimulation with Con A or with monoclonal antibodies to the cells' antigen receptors. In the HTL L2, proliferative responses and production of the lymphokines interleukin 2, interleukin 3, and interferon-gamma were blocked to background levels when CsA was added to cultures at a concentration of 0.1 to 1 microgram/ml. This inhibition of lymphokine production was found to occur at a pretranslational level, because the mRNA for these proteins was not detected when the L2 cells were stimulated in the presence of CsA. In addition, when CsA was added to cultures 3 hr after the cells had first been stimulated with the lectin Con A, levels of mRNA for the lymphokines isolated from the L2 cells 3 hr later were reduced approximately twofold. In the CTL L3, production of lymphokine (interferon-gamma) was also inhibited by CsA at a pretranslational level. However, proliferative responses to maximal stimulation with the clonotypic antibody 384.5 were not inhibited. In both HTL and CTL, the proliferative responses to recombinant IL 2 were not affected. To test whether CsA affects expression and function of the antigen receptor, we studied the effects of the drug on binding of anti-antigen receptor antibodies KJ 16-133 and 384.5 to the cell surfaces and the ability of L3 cells to lyse P815 target cells. At dosages which inhibited lymphokine production, CsA did not compete with binding of KJ 16-133 to L2 cells or 384.5 to L3 cells, as measured by flow cytometry, and the ability of L3 cells to lyse targets was unaffected. We conclude the following. CsA inhibits production of interleukin 2, interleukin 3, and interferon-gamma by L2 cells and interferon-gamma by L3 cells. This appears to occur as a result of a block in the transcription of the lymphokine genes. This pretranslational inhibition of lymphokine production can be invoked after transcription has begun. CsA does not affect expression of the T cell receptor for antigen as measured by monoclonal antibodies reactive with the receptors and by cytolytic activities of cytotoxic lymphocytes. CsA does not affect proliferative responses of HTL and CTL induced by interleukin 2.(ABSTRACT TRUNCATED AT 400 WORDS)

摘要

免疫抑制剂环孢素A(CsA)对T淋巴细胞免疫反应的影响尚未完全明确。先前的许多数据相互矛盾,这可能是由于对细胞总体群体的研究所致。因此,我们研究了CsA对经刀豆蛋白A(Con A)或针对细胞抗原受体的单克隆抗体刺激后的克隆小鼠辅助性T淋巴细胞(HTL)和细胞毒性T淋巴细胞(CTL)的影响。在HTL L2细胞中,当以0.1至1微克/毫升的浓度将CsA添加到培养物中时,增殖反应以及淋巴因子白细胞介素2、白细胞介素3和干扰素-γ的产生被阻断至背景水平。发现这种淋巴因子产生的抑制发生在翻译前水平,因为当L2细胞在CsA存在下受到刺激时,未检测到这些蛋白质的mRNA。此外,当在细胞首先用凝集素Con A刺激3小时后向培养物中添加CsA时,3小时后从L2细胞中分离出的淋巴因子的mRNA水平降低了约两倍。在CTL L3细胞中,淋巴因子(干扰素-γ)的产生也在翻译前水平受到CsA的抑制。然而,对克隆型抗体384.5最大刺激的增殖反应未受抑制。在HTL和CTL中,对重组白细胞介素2的增殖反应均未受影响。为了测试CsA是否影响抗原受体的表达和功能,我们研究了该药物对抗抗原受体抗体KJ 16-133和384.5与细胞表面结合的影响以及L3细胞裂解P815靶细胞的能力。在抑制淋巴因子产生的剂量下,通过流式细胞术测量,CsA不与KJ 16-133与L2细胞的结合或384.5与L3细胞的结合竞争,并且L3细胞裂解靶标的能力未受影响。我们得出以下结论。CsA抑制L2细胞产生白细胞介素2、白细胞介素3和干扰素-γ以及L3细胞产生干扰素-γ。这似乎是由于淋巴因子基因转录受阻所致。这种淋巴因子产生的翻译前抑制可在转录开始后发生。通过与受体反应的单克隆抗体以及细胞毒性淋巴细胞的细胞溶解活性测量,CsA不影响T细胞抗原受体的表达。CsA不影响白细胞介素2诱导的HTL和CTL的增殖反应。(摘要截短至400字)

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