Department of Respiratory Medicine, Laboratory for Translational Research in Obstructive Pulmonary Diseases, Ghent University Hospital, Ghent, Belgium.
J Immunol. 2010 Jan 1;184(1):426-32. doi: 10.4049/jimmunol.0902564. Epub 2009 Nov 30.
Particulate matter, such as diesel exhaust particles (DEPs), modulate adaptive immune responses in the lung; however, their mechanism of action remains largely unclear. Pulmonary dendritic cells (DCs) are crucial mediators in regulating immune responses. We hypothesized that the immunomodulatory effects of DEPs are caused by alteration of DC function. To test this, we instilled mice with DEPs and examined the pulmonary DC recruitment and maturation, their migration to the mediastinal lymph node (MLN), and the subsequent T cell response. We demonstrated that exposure to DEPs increased DC numbers in the bronchoalveolar lavage and the lungs and that DEPs increased the maturation status of these DCs. DEP exposure also enhanced the DC migration to the MLN. Moreover, we showed that DEPs themselves were transported to the MLN in a CCR7- and DC-dependent manner. This resulted in an enhanced T cell recruitment and effector differentiation in the MLN. These data suggest that DEP inhalation modulates immune responses in the lung via stimulation of DC function.
颗粒物，如柴油机尾气颗粒（DEP），可调节肺部的适应性免疫反应；然而，其作用机制在很大程度上尚不清楚。肺部树突状细胞（DC）是调节免疫反应的关键介质。我们假设 DEP 的免疫调节作用是由 DC 功能改变引起的。为了验证这一点，我们向小鼠注入 DEP 并检查了肺部 DC 的募集和成熟、它们向纵隔淋巴结（MLN）的迁移以及随后的 T 细胞反应。我们证明，暴露于 DEP 会增加支气管肺泡灌洗液和肺部的 DC 数量，并且 DEP 会增加这些 DC 的成熟状态。DEP 暴露还增强了 DC 向 MLN 的迁移。此外，我们表明，DEP 本身以 CCR7 和 DC 依赖性方式被转运到 MLN。这导致 MLN 中 T 细胞募集和效应细胞分化增强。这些数据表明，DEP 吸入通过刺激 DC 功能来调节肺部的免疫反应。
