Dendritic cells and alveolar macrophages mediate IL-13-induced airway inflammation and chemokine production.
Dendritic cells and alveolar macrophages mediate IL-13-induced airway inflammation and chemokine production.
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DOI：
10.1016/j.jaci.2012.01.052
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发表时间：
2012-06
影响因子：
14.2
通讯作者：
Kuperman, Douglas A.
中科院分区：
文献类型：
--
作者：
Crapster-Pregont, Margaret;Yeo, Janice;Sanchez, Raquel L.;Kuperman, Douglas A.
关键词：
呼吸道中的IL-13可诱导高度典型的哮喘病理改变，包括黏液化生、气道高反应性(AHR)和气道炎症。因此，重要的是要确定介导上述每一种病理过程的IL-13反应细胞类型。例如，IL-13的S作用于上皮细胞，导致粘液化生和急性呼吸道高反应。IL-13‘S对血管的作用也参与了AHR的发生。然而，目前还很难确定介导IL-13诱导的呼吸道炎症的细胞类型。我们试图确定哪些细胞类型介导了IL-13诱导的呼吸道炎症。我们用IL-13单独或联合干扰素-γ治疗小鼠的呼吸道。我们将干扰素-γ对IL-13诱导的呼吸道炎症和趋化因子产生的抑制作用与肺中共表达IL-13和干扰素-γ受体的细胞类型相关联。然后，我们评估了IL-13在CD11c启动子导向的白喉毒素受体表达的小鼠和CD11b启动子导向的白喉毒素受体表达的白喉毒素受体表达的小鼠中的反应。树突状细胞和肺泡巨噬细胞耗竭保护小鼠免受IL-13诱导的呼吸道炎症和CCL11、CCL24、CCL22和CCL17趋化因子的产生。优先去除树突状细胞可以保护小鼠免受IL-13诱导的呼吸道炎症和CCL22和CCL17趋化因子的产生，但不能保护IL-13诱导的CCL11和CCL24趋化因子的产生。在任何一种情况下，小鼠都没有受到IL-13诱导的AHR和粘液化生的保护。肺树突状细胞和肺泡巨噬细胞介导IL-13诱导的呼吸道炎症和趋化因子的产生。(《过敏与免疫杂志》2012；129：1621-7。)
IL-13 in the airway induces pathologies that are highly characteristic of asthma, including mucus metaplasia, airway hyperreactivity (AHR), and airway inflammation. As such, it is important to identify the IL-13–responding cell types that mediate each of the above pathologies. For example, IL-13’s effects on epithelium contribute to mucus metaplasia and AHR. IL-13’s effects on smooth muscle also contribute to AHR. However, it has been difficult to identify the cell types that mediate IL-13–induced airway inflammation. We sought to determine which cell types mediate IL-13–induced airway inflammation. We treated the airways of mice with IL-13 alone or in combination with IFN-γ. We associated the inhibitory effect of IFN-γ on IL-13–induced airway inflammation and chemokine production with cell types in the lung that coexpress IL-13 and IFN-γ receptors. We then evaluated IL-13–induced responses in CD11c promoter–directed diphtheria toxin receptor–expressing mice that were depleted of both dendritic cells and alveolar macrophages and in CD11b promoter–directed diphtheria toxin receptor– expressing mice that were depleted of dendritic cells. Dendritic cell and alveolar macrophage depletion protected mice from IL-13–induced airway inflammation and CCL11, CCL24, CCL22, and CCL17 chemokine production. Preferential depletion of dendritic cells protected mice from IL-13–induced airway inflammation and CCL22 and CCL17 chemokine production but not from IL-13–induced CCL11 and CCL24 chemokine production. In either case mice were not protected from IL-13–induced AHR and mucus metaplasia. Pulmonary dendritic cells and alveolar macrophages mediate IL-13–induced airway inflammation and chemokine production. (J Allergy Clin Immunol 2012;129:1621-7.)
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影响因子：
64.5
作者：
Geijtenbeek, TBH;Torensma, R;Figdor, CG
通讯作者：
Figdor, CG
过敏原激发期间肺 CD11c+ 树突状细胞的体内耗竭消除了哮喘的特征。
DOI：
10.1084/jem.20042311
发表时间：
2005-03-21
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
van Rijt LS;Jung S;Kleinjan A;Vos N;Willart M;Duez C;Hoogsteden HC;Lambrecht BN
通讯作者：
Lambrecht BN
DOI：
10.1084/jem.191.2.265
发表时间：
2000-01-17
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Lloyd CM;Delaney T;Nguyen T;Tian J;Martinez-A C;Coyle AJ;Gutierrez-Ramos JC
通讯作者：
Gutierrez-Ramos JC
影响因子：
4.4
作者：
Ford, JG;Rennick, D;Grünig, G
通讯作者：
Grünig, G
DOI：
10.4049/jimmunol.1000039
发表时间：
2010-07-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Ge XN;Bahaie NS;Kang BN;Hosseinkhani MR;Ha SG;Frenzel EM;Liu FT;Rao SP;Sriramarao P
通讯作者：
Sriramarao P