Phospholipid scramblase-1 regulates innate type 2 inflammation in mouse lungs via CRTH2-dependent mechanisms.
Phospholipid scramblase-1 regulates innate type 2 inflammation in mouse lungs via CRTH2-dependent mechanisms.
复制标题
磷脂超燃酶-1通过crth2依赖机制调节小鼠肺部先天性2型炎症。
DOI：
10.1172/jci169583
复制
发表时间：
2023-08-01
影响因子：
15.9
通讯作者：
Zhou, Yang
中科院分区：
文献类型：
--
作者：
Hernandez-Gutierrez, Ashley;Majid, Sonoor;Eberle, Adam;Choi, Ashley;Sorkhdini, Parand;Yang, Dongqin;Yang, Alina Xiaoyu;Norbrun, Carmelissa;He, Chuan Hua;Lee, Chun Geun;Elias, Jack A.;Zhou, Yang
Exaggerated Type 2 immune responses play critical roles in the pathogenesis of a variety of diseases including asthma, allergy, and pulmonary fibrosis. Recent studies have highlighted the importance of innate type 2 immune responses and innate lymphoid 2 cells (ILC2s) in these disorders. However, the mechanisms that control the development of pulmonary innate type 2 responses (IT2IR) and the recruitment and/or activation of ILC2 cells are poorly understood. In mouse models of pulmonary IT2IR, we demonstrated that phospholipid scramblase-1 (PLSCR1), a type II transmembrane protein that mediates bidirectional and nonspecific translocation of phospholipids between the inner and outer leaflets of the plasma membrane, was a critical regulator of IT2IR in the lung. We further suggested that (a) PLSCR1 bound to and physically interacted with chemoattractant receptor-homologous molecule(CRTH2), which is a G-protein-coupled receptor that is expressed on TH2 cells and on multiple immune cells and is commonly used to identify ILC2 cells, and (b) the effects of PLSCR1 on ILC2 activation and IT2IR were mediated via CRTH2-dependent mechanisms. Overall, our studies demonstrated that PLSCR1 played an essential role in the pathogenesis of ILC2 responses, providing critical insights into biology and disease pathogenesis and identifying targets that can be manipulated in attempts to control IT2IR in chronic diseases such as asthma.
影响因子：
4.6
作者：
Mutalithas K;Guillen C;Day C;Brightling CE;Pavord ID;Wardlaw AJ
通讯作者：
Wardlaw AJ
DOI：
10.4049/jimmunol.1102474
发表时间：
2012-01-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Xue L;Barrow A;Fleming VM;Hunter MG;Ogg G;Klenerman P;Pettipher R
通讯作者：
Pettipher R
屋尘螨过敏原、卵清蛋白和脂多糖对小鼠致敏建立重度中性粒细胞性哮喘模型的作用比较
影响因子：
2.7
作者：
Jia A;Wang Y;Sun W;Xiao B;Mu L;Wei Y;Xu L;Peng C;Zhang D;Shen H;Xiang X
通讯作者：
Xiang X