Division of Allergy and Clinical Immunology, Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
J Immunol. 2010 Nov 1;185(9):4983-7. doi: 10.4049/jimmunol.1002456. Epub 2010 Sep 27.
The increasing prevalence of atopy and asthma remains unexplained but may be due to infection with respiratory viruses. In support of this hypothesis, we showed that experimental asthma after viral infection in mice depended on type I IFN-driven upregulation of FcεRI on conventional dendritic cells (cDCs) in the lung. In this article, we demonstrate that FcεRI expression on lung cDCs depends on an unexpected activity of a CD49d(+) subset of polymorphonuclear neutrophils (PMNs) that are found in the lungs of wild-type C57BL6 but not mice deficient in type I IFNR. Expression of FcεRI depends in part on a CD11b-dependent interaction between PMNs and cDCs. This study demonstrates a PMN-cDC interaction in the lung that is necessary for the ability of viral infection to induce atopic disease.
特应性和哮喘的发病率不断上升，但原因仍不清楚，可能与呼吸道病毒感染有关。为了支持这一假说，我们表明，在小鼠中，病毒感染后的实验性哮喘依赖于 I 型 IFN 驱动肺内常规树突状细胞 (cDC) 上 FcεRI 的上调。在本文中，我们证明了肺 cDC 上 FcεRI 的表达依赖于一种意想不到的活性，即存在于野生型 C57BL6 肺部但不存在 I 型 IFNR 缺陷型小鼠肺部的 CD49d(+) 多形核粒细胞 (PMN)亚群的活性。FcεRI 的表达部分依赖于 PMN 和 cDC 之间的 CD11b 依赖性相互作用。这项研究证明了肺部 PMN-cDC 相互作用是病毒感染诱导特应性疾病的必要条件。
