title: Low level of LAT-PLC-γ1 interaction is associated with Th2 polarized differentiation: a contributing factor to the etiology of asthma.
abstract: Linker for activation of T cells (LAT) is a key adaptor in the T cell receptor (TCR) signaling pathway. The expression of LAT is lower in asthmatic patients than that in healthy people, but there is little knowledge about the mechanism underlying this phenomenon. This study was aimed to determine whether LAT-PLC-γ1 interaction was involved in the development of asthma. It was shown that the phosphorylation of PLC-γ1 decreased in the asthmatic mouse model and Th2 cell differentiated CD4(+) T cells. In addition, depleted endogenous PLC-γ1 promoted CD4(+) T cells to differentiate into IL-4-Productor. It was therefore concluded that the low level of LAT-PLC-γ1 interaction was associated with Th2 polarized differentiation, and this may contribute to the etiology of asthma.
authors: Department of Respiratory Medicine, Xinhua Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China.
authors: Xiaohua
authors: X
authors: Peng
authors: Department of Respiratory Medicine, Xinhua Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China.
authors: Zhilei
authors: Z
authors: Cui
authors: Department of Respiratory Medicine, Xinhua Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China.
authors: Wen
authors: W
authors: Gu
authors: Department of Respiratory Medicine, Xinhua Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China. Electronic address: xuweiguo@xinhuamed.com.cn.
authors: Weiguo
authors: W
authors: Xu
authors: Department of Respiratory Medicine, Xinhua Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China. Electronic address: snowgen@126.com.
authors: Xuejun
authors: X
authors: Guo
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000096:biosynthesis / Q000378:metabolism*; D000818:Animals; D001249:Asthma / Q000209:etiology / Q000276:immunology*; D016535:Bronchial Hyperreactivity / Q000276:immunology*; D002454:Cell Differentiation / Q000276:immunology; D002478:Cells, Cultured; D005260:Female; D015847:Interleukin-4 / Q000096:biosynthesis / Q000276:immunology; D008213:Lymphocyte Activation / Q000276:immunology; D008565:Membrane Proteins / Q000096:biosynthesis / Q000378:metabolism*; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin; D051966:Phospholipase C gamma / Q000096:biosynthesis / Q000378:metabolism*; D010750:Phosphoproteins / Q000096:biosynthesis / Q000378:metabolism*; D010766:Phosphorylation / Q000276:immunology; D015398:Signal Transduction / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology*
chemical_list: D048868:Adaptor Proteins, Signal Transducing; C491734:Lat protein, mouse; D008565:Membrane Proteins; D010750:Phosphoproteins; D015847:Interleukin-4; D010047:Ovalbumin; D051966:Phospholipase C gamma
keywords: Asthma; LAT; PLC-γ1; Th2 cell