Institute of Immunology, Taishan Medical University, Taian, 271000, Shandong, China.
School of Basic Medical Sciences, Taishan Medical University, Taian, 271000, Shandong, China.
Nat Commun. 2018 Sep 24;9(1):3879. doi: 10.1038/s41467-018-06316-9.
Eosinophil infiltration, a hallmark of allergic asthma, is essential for type 2 immune responses. How the initial eosinophil recruitment is regulated by lung dendritic cell (DC) subsets during the memory stage after allergen challenge is unclear. Here, we show that the initial eosinophil infiltration is dependent on lung cDC1s, which require nitric oxide (NO) produced by inducible NO synthase from lung CD24CD11b DC2s for inducing CCL17 and CCL22 to attract eosinophils. During late phase responses after allergen challenge, lung CD24 cDC2s inhibit eosinophil recruitment through secretion of TGF-β1, which impairs the expression of CCL17 and CCL22. Our data suggest that different lung antigen-presenting cells modulate lung cDC1-mediated eosinophil recruitment dynamically, through secreting distinct soluble factors during the memory stage of chronic asthma after allergen challenge in the mouse.
嗜酸性粒细胞浸润是过敏哮喘的一个标志，对 2 型免疫反应至关重要。在过敏原刺激后的记忆阶段，肺树突状细胞 (DC) 亚群如何调节初始嗜酸性粒细胞募集尚不清楚。在这里，我们表明初始嗜酸性粒细胞浸润依赖于肺 cDC1，其需要由肺 CD24CD11b DC2 中诱导型一氧化氮合酶产生的一氧化氮来诱导 CCL17 和 CCL22 吸引嗜酸性粒细胞。在过敏原刺激后的晚期反应中，肺 CD24 cDC2 通过分泌 TGF-β1 抑制嗜酸性粒细胞募集，从而损害 CCL17 和 CCL22 的表达。我们的数据表明，不同的肺抗原呈递细胞通过在过敏原刺激后慢性哮喘的记忆阶段分泌不同的可溶性因子，动态调节肺 cDC1 介导的嗜酸性粒细胞募集。
