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脱髓鞘疾病中的β2 整合素:不遵循范式。

beta2-integrins in demyelinating disease: not adhering to the paradigm.

机构信息

Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.

出版信息

J Leukoc Biol. 2010 Mar;87(3):397-403. doi: 10.1189/jlb.1009654. Epub 2009 Dec 9.

DOI:10.1189/jlb.1009654
PMID:20007244
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3212424/
Abstract

The beta(2)-integrins are a subfamily of integrins expressed on leukocytes that play an essential role in leukocyte trafficking, activation, and many other functions. Studies in EAE, the animal model for multiple sclerosis, show differential requirements for beta(2)-integrins in this disease model, ranging from critical in the case of LFA-1 (CD11a/CD18) to unimportant in the case of CD11d/CD18. Importantly, expression of beta(2)-integrins on T cell subsets provides some clues as to the function(s) these adhesion molecules play in disease development. For example, transferred EAE studies have shown that Mac-1 (CD11b/CD18) expression on alphabeta T cells is critical for disease development, and the absence of LFA-1 on Tregs in recipient mice results in exacerbated disease. In this review, we summarize recent findings regarding the role of beta(2)-integrins in demyelinating disease and new information about the role of beta(2)-integrins with respect to alterations in Treg numbers and function. In addition, we discuss the potential for targeting beta(2)-integrins in human demyelinating disease in light of the recent animal model studies.

摘要

β2 整合素是整合素家族的一个亚家族,在白细胞上表达,在白细胞迁移、激活和许多其他功能中发挥着重要作用。EAE(多发性硬化症的动物模型)的研究表明,β2 整合素在该疾病模型中的作用存在差异,从 LFA-1(CD11a/CD18)的关键作用到 CD11d/CD18 的不重要作用不等。重要的是,T 细胞亚群上β2 整合素的表达为这些粘附分子在疾病发展中所起的作用提供了一些线索。例如,转移 EAE 研究表明,Mac-1(CD11b/CD18)在 αβ T 细胞上的表达对于疾病的发展至关重要,而接受者小鼠中 Treg 上缺乏 LFA-1 会导致疾病恶化。在这篇综述中,我们总结了最近关于β2 整合素在脱髓鞘疾病中的作用的发现,以及关于β2 整合素与 Treg 数量和功能改变的作用的新信息。此外,我们还根据最近的动物模型研究讨论了针对人类脱髓鞘疾病靶向β2 整合素的潜力。

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