Medoff Benjamin D, Thomas Seddon Y, Luster Andrew D
Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA.
Annu Rev Immunol. 2008;26:205-32. doi: 10.1146/annurev.immunol.26.021607.090312.
T cells are critical mediators of the allergic airway inflammation seen in asthma. Pathogenic allergen-specific T cells are generated in regional lymph nodes and are then recruited into the airway by chemoattractants produced by the asthmatic lung. These recruited effector T cells and their products then mediate the cardinal features of asthma: airway eosinophilia, mucus hypersecretion, and airway hyperreactivity. There has been considerable progress in delineating the molecular mechanisms that control T cell trafficking into peripheral tissue, including the asthmatic lung. In this review, we summarize these advances and formulate them into a working model that proposes that T cell trafficking into and out of the allergic lung is controlled by several discrete regulatory pathways that involve the collaboration of innate and acquired immune cells.
T细胞是哮喘中过敏性气道炎症的关键介质。致病性过敏原特异性T细胞在区域淋巴结中产生,然后被哮喘肺产生的趋化因子募集到气道中。这些募集的效应T细胞及其产物随后介导哮喘的主要特征:气道嗜酸性粒细胞增多、黏液分泌过多和气道高反应性。在阐明控制T细胞向包括哮喘肺在内的外周组织迁移的分子机制方面已经取得了相当大的进展。在这篇综述中,我们总结了这些进展,并将其形成一个工作模型,该模型提出T细胞进出过敏性肺的迁移受几种离散的调节途径控制,这些途径涉及先天免疫细胞和获得性免疫细胞的协作。