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新型免疫抑制剂FK506对人淋巴细胞体外反应的影响。II. 抑制白细胞介素-2和γ-干扰素的产生,但不抑制B细胞刺激因子2。

Effect of a new immunosuppressive agent, FK506, on human lymphocyte responses in vitro. II. Inhibition of the production of IL-2 and gamma-IFN, but not B cell-stimulating factor 2.

作者信息

Yoshimura N, Matsui S, Hamashima T, Oka T

机构信息

Second Department of Surgery, Kyoto Prefectural University of Medicine, Japan.

出版信息

Transplantation. 1989 Feb;47(2):356-9. doi: 10.1097/00007890-198902000-00035.

Abstract

The mechanism whereby FK506 inhibits immune responses was assessed in in vitro human studies. FK506 inhibited in a dose-dependent manner both interleukin 2 and gamma-interferon secretion of PBMC stimulated with PHA. Complete inhibition was obtained at the concentration of 0.25 nM of FK506 for IL-2 and 1 nM of FK506 for gamma-IFN production. Inhibition of 50% (IC50) was detected with 0.06 nM for IL-2 and 0.25 nM for gamma-IFN production. On the other hand, FK506 could not inhibit the B cell-stimulating factor 2 (BSF-2) production of PBMC, indicating the possibility that FK506 might spare the B cell function. Cloned T cells and cloned B cells, once activated, were scarcely affected by the agent; neither IL-2-driven proliferation of cloned T cells nor BSF-2-driven proliferation of cloned B cells was inhibited by FK506 at any concentration.

摘要

在体外人体研究中评估了FK506抑制免疫反应的机制。FK506以剂量依赖的方式抑制了用植物血凝素(PHA)刺激的外周血单核细胞(PBMC)的白细胞介素2和γ-干扰素的分泌。对于白细胞介素2,在FK506浓度为0.25 nM时获得完全抑制,对于γ-干扰素产生,在FK506浓度为1 nM时获得完全抑制。对于白细胞介素2的产生,在0.06 nM时检测到50%抑制(IC50),对于γ-干扰素产生,在0.25 nM时检测到50%抑制。另一方面,FK506不能抑制PBMC的B细胞刺激因子2(BSF-2)的产生,这表明FK506可能保留B细胞功能。克隆的T细胞和克隆的B细胞一旦被激活,几乎不受该药物影响;在任何浓度下,FK506都不会抑制克隆T细胞的白细胞介素2驱动的增殖或克隆B细胞的BSF-2驱动的增殖。

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