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IL-33 promotes the egress of group 2 innate lymphoid cells from the bone marrow.
Journal of Experimental Medicine ( IF 15.3 ) Pub Date : 2017-12-08 , DOI: 10.1084/jem.20170449
Matthew T Stier 1 , Jian Zhang 2 , Kasia Goleniewska 2 , Jacqueline Y Cephus 2 , Mark Rusznak 2 , Lan Wu 1 , Luc Van Kaer 1 , Baohua Zhou 3 , Dawn C Newcomb 1, 2 , R Stokes Peebles 2, 4
Affiliation  

Group 2 innate lymphoid cells (ILC2s) are effector cells within the mucosa and key participants in type 2 immune responses in the context of allergic inflammation and infection. ILC2s develop in the bone marrow from common lymphoid progenitor cells, but little is known about how ILC2s egress from the bone marrow for hematogenous trafficking. In this study, we identified a critical role for IL-33, a hallmark peripheral ILC2-activating cytokine, in promoting the egress of ILC2 lineage cells from the bone marrow. Mice lacking IL-33 signaling had normal development of ILC2s but retained significantly more ILC2 progenitors in the bone marrow via augmented expression of CXCR4. Intravenous injection of IL-33 or pulmonary fungal allergen challenge mobilized ILC2 progenitors to exit the bone marrow. Finally, IL-33 enhanced ILC2 trafficking to the lungs in a parabiosis mouse model of tissue disruption and repopulation. Collectively, these data demonstrate that IL-33 plays a critical role in promoting ILC2 egress from the bone marrow.

中文翻译:

IL-33促进第2组先天性淋巴样细胞从骨髓中流出。

第2组先天淋巴样细胞(ILC2)是粘膜内的效应细胞,是变态反应性炎症和感染中2型免疫反应的主要参与者。ILC2s由常见的淋巴样祖细胞在骨髓中发育,但对ILC2s如何从骨髓中流出以进行血源性运输的了解甚少。在这项研究中,我们确定了IL-33(一种标志性的外周ILC2活化细胞因子)在促进ILC2谱系细胞从骨髓中流出方面的关键作用。缺乏IL-33信号传导的小鼠具有正常的ILC2发育,但是通过CXCR4的增强表达在骨髓中保留了明显更多的ILC2祖细胞。静脉注射IL-33或肺部真菌过敏原激发动员的ILC2祖细胞离开骨髓。最后,IL-33增强了组织破坏和繁殖的共生小鼠模型中ILC2向肺的运输。总体而言,这些数据表明,IL-33在促进ILC2从骨髓流出中起关键作用。
更新日期:2018-01-02
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