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白细胞介素2和白细胞介素5诱导调节因子与J链基因启动子结合的变化。

Interleukin 2- and interleukin 5-induced changes in the binding of regulatory factors to the J-chain gene promoter.

作者信息

McFadden H J, Koshland M E

机构信息

Department of Molecular and Cell Biology, University of California, Berkeley 94720.

出版信息

Proc Natl Acad Sci U S A. 1991 Dec 15;88(24):11027-31. doi: 10.1073/pnas.88.24.11027.

DOI:10.1073/pnas.88.24.11027
PMID:1763018
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC53066/
Abstract

In a primary immune response, B cells require signals from the T-cell lymphokines interleukins 2 and 5 (IL-2 and IL-5) to develop into IgM-secreting cells. One role of IL-2 and IL-5 is to activate transcription of the gene encoding the IgM joining component, the J chain. In this study the activation mechanism was investigated by using an inducible beta-lymphoma cell line to examine J-chain RNA expression and factor binding to the J-chain promoter. The analyses revealed that both IL-2 and IL-5 trigger a decrease in the binding of two promoter-specific nuclear proteins that precedes the appearance of J-chain RNA. In combination the two lymphokines effected nearly additive changes in factor binding and J-chain RNA abundance. Both effects were reversed upon withdrawal of the lymphokine stimulus and both were inhibited in the presence of the T-cell lymphokine IL-4. These findings indicate that the IL-2 and IL-5 signal pathways converge to deliver a common signal that regulates the repressor activities of two lymphokine-responsive promoter elements.

摘要

在初次免疫应答中，B细胞需要来自T细胞淋巴因子白细胞介素2和5（IL-2和IL-5）的信号才能发育成分泌IgM的细胞。IL-2和IL-5的一个作用是激活编码IgM连接成分J链的基因的转录。在本研究中，通过使用一种可诱导的β淋巴瘤细胞系来检测J链RNA表达以及因子与J链启动子的结合，对激活机制进行了研究。分析显示，在J链RNA出现之前，IL-2和IL-5都会引发两种启动子特异性核蛋白结合的减少。两种淋巴因子共同作用时，在因子结合和J链RNA丰度方面产生了几乎相加的变化。在撤除淋巴因子刺激后，这两种效应都被逆转，并且在T细胞淋巴因子IL-4存在的情况下，这两种效应都受到抑制。这些发现表明，IL-2和IL-5信号通路汇聚以传递一个共同信号，该信号调节两种淋巴因子反应性启动子元件的阻遏物活性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f36/53066/b155e5aea594/pnas01074-0059-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f36/53066/47ad31ca5ebd/pnas01074-0058-a.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f36/53066/b155e5aea594/pnas01074-0059-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f36/53066/47ad31ca5ebd/pnas01074-0058-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f36/53066/319bea32bf48/pnas01074-0058-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f36/53066/64717d02b5ab/pnas01074-0058-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f36/53066/06b6d2072276/pnas01074-0058-d.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f36/53066/aa316dff637d/pnas01074-0058-e.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f36/53066/94d5a9287d60/pnas01074-0058-f.jpg
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本文引用的文献

1
Cytoplasmic dot hybridization. Simple analysis of relative mRNA levels in multiple small cell or tissue samples.细胞质斑点杂交。对多个小细胞或组织样本中相对mRNA水平的简单分析。
J Biol Chem. 1982 Aug 10;257(15):8569-72.
2
Primary structure of the immunoglobulin J chain from the mouse.小鼠免疫球蛋白J链的一级结构。
Proc Natl Acad Sci U S A. 1982 Nov;79(21):6656-60. doi: 10.1073/pnas.79.21.6656.
3
Lymphokine-induced IgM secretion by clones of neoplastic B cells.肿瘤性B细胞克隆产生的淋巴因子诱导的IgM分泌。
一种对白介素2反应性J链基因发挥正调控和负调控作用的启动子元件。
Proc Natl Acad Sci U S A. 1992 Jul 1;89(13):5966-70. doi: 10.1073/pnas.89.13.5966.
Nature. 1983 Apr 28;302(5911):825-6. doi: 10.1038/302825a0.
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Ig RNA expression in normal B cells stimulated with anti-IgM antibody and T cell-derived growth and differentiation factors.用抗IgM抗体以及T细胞衍生的生长和分化因子刺激正常B细胞时的Ig RNA表达。
J Exp Med. 1984 Dec 1;160(6):1736-51. doi: 10.1084/jem.160.6.1736.
5
Both interleukin 2 and a second T cell-derived factor in EL-4 supernatant have activity as differentiation factors in IgM synthesis.白细胞介素2和EL-4上清液中第二种T细胞衍生因子在IgM合成中均具有作为分化因子的活性。
J Exp Med. 1984 Dec 1;160(6):1605-21. doi: 10.1084/jem.160.6.1605.
6
Receptors for T cell-replacing factor/interleukin 5. Specificity, quantitation, and its implication.T细胞替代因子/白细胞介素5的受体。特异性、定量及其意义。
J Exp Med. 1988 Sep 1;168(3):863-78. doi: 10.1084/jem.168.3.863.
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Interleukin 4 counteracts the interleukin 2-induced proliferation of monoclonal B cells.白细胞介素4可抵消白细胞介素2诱导的单克隆B细胞增殖。
J Exp Med. 1988 Jul 1;168(1):85-94. doi: 10.1084/jem.168.1.85.
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