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Lei, Ai-Hua; Xiao, Qiang; Liu, Gao-Yu; Shi, Kun; Yang, Qiong; Li, Xing; Liu, Yu-Feng; Wang, Hai-Kun; Cai, Wei-Ping; Guan, Yu-Juan; Gabrilovich, Dmitry I; Zhou, Jie
The Journal of experimental medicine, 08/2018, Volume: 215, Issue: 8Journal Article
Group 2 innate lymphoid cells (ILC2s) are emerging as key players in the pathogenesis of allergic airway inflammation. The mechanisms regulating ILC2, however, are not fully understood. Here, we found that ICAM-1 is required for the development and function of ILC2. ICAM-1-deficient ( ) mice displayed significantly lower levels of ILC2s in the bone marrow and peripheral tissues than wild-type controls. CLP transfer and in vitro culture assays revealed that the regulation of ILC2 by ICAM-1 is cell intrinsic. Furthermore, ILC2s from mice were functionally impaired, as indicated by the diminished production of type-2 cytokines in response to IL-33 challenge. The reduction in lung ILC2s caused a clear remission of airway inflammation in mice after administration of papain or We further demonstrate that ILC2 defects caused by ICAM-1 deficiency are due to ERK signaling-dependent down-regulation of GATA3 protein. Collectively, these observations identify ICAM-1 as a novel regulator of ILC2.
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