Scaffolding protein Gab1 regulates myeloid dendritic cell migration in allergic asthma

التفاصيل البيبلوغرافية
العنوان: Scaffolding protein Gab1 regulates myeloid dendritic cell migration in allergic asthma
المؤلفون: Shuwan Liu, Chunlai Zeng, Yi Ting Zhou, Kaijun Li, Yuehai Ke, Dong Cen, Yun Zhang, Linrong Lu, Jiaqi Xu, Xiaohong Guo, Hongqiang Cheng, Xue Zhang, Huahao Shen, Heyuan Li, Yun Xu
المصدر: Cell Research. 26:1226-1241
بيانات النشر: Springer Science and Business Media LLC, 2016.
سنة النشر: 2016
مصطلحات موضوعية: 0301 basic medicine, Chemokine, Myeloid, biology, CCL19, C-C chemokine receptor type 7, Cell Biology, medicine.disease, Peripheral blood mononuclear cell, Allergic inflammation, Pathogenesis, 03 medical and health sciences, 030104 developmental biology, medicine.anatomical_structure, Immunology, biology.protein, medicine, Original Article, Molecular Biology, Asthma
الوصف: Asthma is a common allergic disorder involving a complex interplay among multiple genetic and environmental factors. Recent studies identified genetic variants of human GAB1 as a novel asthma susceptibility factor. However, the functions of Gab1 in lung remain largely unexplored. In this study, we first observed an elevation of Gab1 level in peripheral blood mononuclear cells from asthmatic patients during acute exacerbation compared with convalescence. Mice with a selectively disrupted Gab1 in myeloid dendritic cells (mDCs) considerably attenuated allergic inflammation in experimental models of asthma. Further investigations revealed a prominent reduction in CCL19-mediated migration of Gab1-deficient mDCs to draining lymph nodes and subsequent impairment of Th2-driven adaptive activation. Mechanistically, Gab1 is an essential component of the CCL19/CCR7 chemokine axis that regulates mDC migration during asthmatic responses. Together, these findings provide the first evidence for the roles of Gab1 in lung, giving us deeper understanding of asthmatic pathogenesis.
تدمد: 1748-7838
1001-0602
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b3d59904efdbadeddce7e0f7d0aa9382Test
https://doi.org/10.1038/cr.2016.124Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....b3d59904efdbadeddce7e0f7d0aa9382
قاعدة البيانات: OpenAIRE