Rheostat regulation of integrin-mediated leukocyte adhesion.
Rheostat regulation of integrin-mediated leukocyte adhesion.
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DOI：
10.1172/jci33376
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发表时间：
2007-09
期刊：
影响因子：
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通讯作者：
I. Douglas;T. Dassopoulos
中科院分区：
文献类型：
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作者：
I. Douglas;T. Dassopoulos
在炎症性肠病中，活化的T淋巴细胞归巢到肠道依赖于它们与基质和血管壁的协调的、整合素介导的粘附和去粘附。在本期JCI中，Park及其同事揭示了β整合素内的结合位点（称为ADMIDAS结构域）在控制小鼠整合素去粘附中的关键调节作用（参见2526页开始的相关文章）。这些观察结果增加了我们对整合素β是如何调节的理解，并提出了淋巴细胞归巢的生物变阻器存在的概念。紊乱的迁移变阻器音调可以解释在炎症性肠病或其他淋巴细胞介导的炎症性疾病患者中观察到的个体间免疫应答的变化。这些发现将为未来的策略提供信息，以设计用于治疗一系列慢性炎症疾病的小分子。
The homing of activated T lymphocytes to the gut in inflammatory bowel diseases is dependent on their coordinated, integrin-mediated adhesion and de-adhesion to substrates and blood vessel walls. In this issue of the JCI, Park and colleagues reveal a key modulatory role of a binding site within beta integrins, known as the ADMIDAS domain, in controlling integrin de-adhesion in mice (see the related article beginning on page 2526). These observations add to our growing understanding of how integrin adhesiveness is regulated and raise the notion of the existence of a biological rheostat for lymphocyte homing. Disturbed migratory rheostat tone could account for variations in interindividual immune responses observed in patients with inflammatory bowel disease or other lymphocyte-mediated inflammatory disorders. These findings will inform future strategies to design small molecules for the treatment of a spectrum of chronic inflammatory conditions.