IL-17 regulates DC migration to the peribronchial LNs and allergen presentation in experimental allergic asthma.,European Journal of Immunology

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IL-17 regulates DC migration to the peribronchial LNs and allergen presentation in experimental allergic asthma.
European Journal of Immunology ( IF 4.5 ) Pub Date : 2020-03-06 , DOI: 10.1002/eji.201948409
Adan Chari Jirmo _{1,

2} , Mandy Busse ₃ , Christine Happle _{1,

2} , Jelena Skuljec _{1,

2} , Kathleen Dalüge ₁ , Anika Habener _{1,

2} , Ruth Grychtol _{1,

2} , David S DeLuca ₂ , Oliver D Breiholz ₄ , Immo Prinz ₅ , Gesine Hansen _{1,

2,

6}

Affiliation

IL‐17 is associated with different phenotypes of asthma, however, it is not fully elucidated how it influences induction and maintenance of asthma and allergy. In order to determine the role of IL‐17 in development of allergic asthma, we used IL‐17A/F double KO (IL‐17A/F KO) and WT mice with or without neutralization of IL‐17 in an experimental allergic asthma model and analyzed airway hyperresponsiveness, lung inflammation, T helper cell polarization, and DCs influx and activation. We report that the absence of IL‐17 reduced influx of DCs into lungs and lung draining LNs. Compared to WT mice, IL‐17A/F KO mice or WT mice after neutralization of IL‐17A showed reduced airway hyperresponsiveness, eosinophilia, mucus hypersecretion, and IgE levels. DCs from draining LNs of allergen‐challenged IL‐17A/F KO mice showed a reduction in expression of migratory and costimulatory molecules CCR7, CCR2, MHC‐II, and CD40 compared to WT DCs. Moreover, in vivo stimulation of adoptively transferred antigen‐specific cells was attenuated in lung‐draining LNs in the absence of IL‐17. Thus, we report that IL‐17 enhances airway DC activation, migration, and function. Consequently, lack of IL‐17 leads to reduced antigen‐specific T cell priming and impaired development of experimental allergic asthma.

中文翻译：

IL-17调节实验性过敏性哮喘中DC向支气管周围LN的迁移和过敏原呈递。

IL-17与哮喘的不同表型有关，但是，尚未完全阐明它如何影响哮喘的诱导和维持以及过敏。为了确定IL-17在过敏性哮喘发展中的作用，我们在实验性过敏性哮喘模型中使用了IL-17A / F双KO（IL-17A / F KO）和WT小鼠，其中有或没有中和IL-17并分析了气道高反应性，肺部炎症，T辅助细胞极化以及DC流入和活化。我们报告说，IL-17的缺乏减少了DC流入肺和引流LN的DC。与WT小鼠相比，IL-17A / F KO小鼠或中和IL-17A后的WT小鼠显示气道高反应性，嗜酸性粒细胞增多，粘液分泌过多和IgE水平降低。与野生型DC相比，变态反应激发的IL-17A / F KO小鼠的引流LN的DC显示出迁移和共刺激分子CCR7，CCR2，MHC-II和CD40的表达减少。此外，在没有IL-17的情况下，肺引流LN中对过继转移的抗原特异性细胞的体内刺激减弱。因此，我们报告说IL-17增强了气道DC的激活，迁移和功能。因此，缺乏IL-17会导致抗原特异性T细胞引发减少和实验性过敏性哮喘的发展受损。

更新日期：2020-03-06

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