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肿瘤坏死因子-α通过硫酸化诱导CD44介导的白细胞黏附。

TNF-alpha induction of CD44-mediated leukocyte adhesion by sulfation.

作者信息

Maiti A, Maki G, Johnson P

机构信息

Department of Microbiology and Immunology, University of British Columbia, 300-6174 University Boulevard, Vancouver, B.C. V6T 1Z3, Canada.

出版信息

Science. 1998 Oct 30;282(5390):941-3. doi: 10.1126/science.282.5390.941.

Abstract

Regulation of cell adhesion is important for immune system function. CD44 is a tightly regulated cell adhesion molecule present on leukocytes and implicated in their attachment to endothelium during an inflammatory immune response. The proinflammatory cytokine tumor necrosis factor-alpha, but not interferon-gamma, was found to convert CD44 from its inactive, nonbinding form to its active form by inducing the sulfation of CD44. This posttranslational modification was required for CD44-mediated binding to the extracellular matrix component hyaluronan and to vascular endothelial cells. Sulfation is thus a potential means of regulating CD44-mediated leukocyte adhesion at inflammatory sites.

摘要

细胞黏附的调节对免疫系统功能很重要。CD44是一种受严格调控的细胞黏附分子,存在于白细胞上,在炎症免疫反应期间参与白细胞与内皮细胞的黏附。研究发现,促炎细胞因子肿瘤坏死因子-α而非干扰素-γ,可通过诱导CD44的硫酸化,将其从无活性的非结合形式转变为活性形式。这种翻译后修饰是CD44介导与细胞外基质成分透明质酸及血管内皮细胞结合所必需的。因此,硫酸化是在炎症部位调节CD44介导的白细胞黏附的一种潜在方式。

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