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霍乱毒素的黏膜佐剂活性涉及通过选择性上调B7.2表达来增强共刺激活性。

The mucosal adjuvanticity of cholera toxin involves enhancement of costimulatory activity by selective up-regulation of B7.2 expression.

作者信息

Cong Y, Weaver C T, Elson C O

机构信息

Department of Medicine, University of Alabama, Birmingham 35294-0007, USA.

出版信息

J Immunol. 1997 Dec 1;159(11):5301-8.

PMID:9548469
Abstract

Cholera toxin (CT) is a potent mucosal immunogen and adjuvant that can strongly prime mucosal T cells. The present study was undertaken to investigate the effects of CT on the expression and functional activity of the costimulatory molecules B7.1 and B7.2 on macrophages and the relationship of these effects to the mucosal adjuvanticity of CT. Bone marrow macrophages (BMM) were generated by culturing bone marrow with macrophage CSF or granulocyte-macrophage CSF. After treatment with either CT alone or IFN-gamma alone, B7.2 expression on BMM was moderately up-regulated and was further increased when BMM were treated with both CT and IFN-gamma together. Interestingly, CT had no effect on B7.1 expression despite the close relationship between these two molecules. Up-regulation of B7.2 expression by CT was mediated by intracellular cAMP production, in that CT-B subunit had no effect and dibutyryl cAMP could mimic the effect. CT increased functional costimulatory activity of macrophages for both anti-CD3-stimulated and allostimulated T cells, an increase that was blocked by anti-B7.2, but not anti-B7.1, Ab. B7.2 expression by Mac1+ Peyer's patch cells was increased after intraluminal exposure to CT in vivo. Treatment of mice with anti-B7.2 Ab in vivo inhibited both the mucosal adjuvanticity and the immunogenicity of CT. We conclude that CT enhances the costimulatory activity of mucosal APC by differentially up-regulating B7.2 expression, an effect that appears to be important for its mucosal adjuvanticity and immunogenicity.

摘要

霍乱毒素(CT)是一种强效的黏膜免疫原和佐剂,能够强烈启动黏膜T细胞。本研究旨在探讨CT对巨噬细胞共刺激分子B7.1和B7.2表达及功能活性的影响,以及这些影响与CT黏膜佐剂性的关系。通过用巨噬细胞集落刺激因子(CSF)或粒细胞-巨噬细胞CSF培养骨髓来生成骨髓巨噬细胞(BMM)。单独用CT或单独用γ干扰素处理后,BMM上的B7.2表达适度上调,当BMM同时用CT和γ干扰素处理时进一步增加。有趣的是,尽管这两种分子关系密切,但CT对B7.1表达没有影响。CT对B7.2表达的上调是由细胞内cAMP产生介导的,因为CT-B亚基没有作用,而二丁酰cAMP可模拟这种作用。CT增强了巨噬细胞对抗CD3刺激的和同种异体刺激的T细胞的功能性共刺激活性,这种增加被抗B7.2抗体阻断,但不被抗B7.1抗体阻断。在体内管腔内暴露于CT后,Mac1+派尔集合淋巴结细胞的B7.2表达增加。在体内用抗B7.2抗体处理小鼠可抑制CT的黏膜佐剂性和免疫原性。我们得出结论,CT通过差异性上调B7.2表达来增强黏膜抗原呈递细胞的共刺激活性,这一作用似乎对其黏膜佐剂性和免疫原性很重要。

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