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肿瘤坏死因子-α调节白细胞介素-4诱导的人单核细胞FcεRII/CD23基因表达及可溶性FcεRII释放。

TNF-alpha regulates IL-4-induced Fc epsilon RII/CD23 gene expression and soluble Fc epsilon RII release by human monocytes.

作者信息

Hashimoto S, Koh K, Tomita Y, Amemiya E, Sawada S, Yodoi J, Horie T

机构信息

First Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.

出版信息

Int Immunol. 1995 May;7(5):705-13. doi: 10.1093/intimm/7.5.705.

Abstract

We examined the regulatory effects of TNF-alpha on IL-4-induced gene expression of the low-affinity receptor for IgE (Fc epsilon RII/CD23) in human monocytes and IL-4-induced soluble Fc epsilon RII (sFc epsilon RII) release from monocytes. IL-4-induced Fc epsilon RII expression on the surface of monocytes was reduced by TNF-alpha as early as 1 day after culture and the effect of TNF-alpha increased with prolonged culture. The present analysis was designed to examine whether or not TNF-alpha could suppress IL-4-induced Fc epsilon RII mRNA expression and enhanced IL-4-induced sFc epsilon RII release. The addition of TNF-alpha to monocyte cultures with IL-4 significantly reduced Fc epsilon RII expression on the surface of monocytes and significantly increased sFc epsilon RII release from monocytes. Over time, there was an inverse relationship between the disappearance of cell surface Fc epsilon RII and the appearance of sFc epsilon RII in culture supernatants. Fc epsilon RII mRNA expression in monocytes cultured with IL-4 was not affected by TNF-alpha when examined at 6 h after cultivation. When the cells were cultured with TNF-alpha for more than 24 h, however, TNF-alpha down-regulated IL-4-induced Fc epsilon RII mRNA levels. This correlated with the kinetics of down-regulation of IL-4-induced Fc epsilon RII expression on the surface of monocytes by TNF-alpha.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

我们研究了肿瘤坏死因子-α(TNF-α)对白细胞介素-4(IL-4)诱导的人单核细胞中IgE低亲和力受体(FcεRII/CD23)基因表达以及IL-4诱导的单核细胞可溶性FcεRII(sFcεRII)释放的调节作用。早在培养1天后,TNF-α就可降低IL-4诱导的单核细胞表面FcεRII表达,且随着培养时间延长,TNF-α的作用增强。本分析旨在研究TNF-α是否能抑制IL-4诱导的FcεRII mRNA表达并增强IL-4诱导的sFcεRII释放。在含IL-4的单核细胞培养物中添加TNF-α可显著降低单核细胞表面FcεRII表达,并显著增加单核细胞sFcεRII释放。随着时间推移,培养上清液中细胞表面FcεRII的消失与sFcεRII的出现呈负相关。培养6小时时,用IL-4培养的单核细胞中FcεRII mRNA表达不受TNF-α影响。然而,当细胞与TNF-α一起培养超过24小时时,TNF-α下调了IL-4诱导的FcεRII mRNA水平。这与TNF-α对IL-4诱导的单核细胞表面FcεRII表达下调的动力学相关。(摘要截短于250字)

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