哮喘中的T细胞迁移：脂质介质为其提供便利。

T-cell trafficking in asthma: lipid mediators grease the way.

作者信息

Luster Andrew D, Tager Andrew M

机构信息

Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Building 149-8301, 13th Street, Charlestown, Massachusetts 02129, USA.

出版信息

Nat Rev Immunol. 2004 Sep;4(9):711-24. doi: 10.1038/nri1438.

DOI:10.1038/nri1438

PMID:15343370

Abstract

Recruitment of T cells to the airways is crucial in the pathogenesis of asthma, and it is thought to be mediated mainly by peptide chemokines. By contrast, lipid mediators such as leukotrienes and prostaglandins have classically been thought to contribute to asthma pathogenesis by other mechanisms. However, as we discuss here, the recent molecular identification of leukotriene and prostaglandin receptors, as well as the generation of mice that are genetically deficient in them, has revealed that two of these lipids - leukotriene B(4) and prostaglandin D(2) - also direct T-cell migration and seem to cooperate with chemokines in a non-redundant, sequential manner to recruit T cells to the airways in asthma.

摘要

T细胞向气道募集在哮喘发病机制中至关重要，并且认为主要由肽趋化因子介导。相比之下，脂质介质如白三烯和前列腺素传统上被认为通过其他机制促成哮喘发病机制。然而，正如我们在此所讨论的，最近对白三烯和前列腺素受体的分子鉴定，以及缺乏这些受体的基因敲除小鼠的产生，揭示了其中两种脂质——白三烯B4和前列腺素D2——也可直接引导T细胞迁移，并且似乎与趋化因子以非冗余、顺序性的方式协同作用，将T细胞募集到哮喘患者的气道中。