| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2167054 | Cellular Immunology | 2014 | 7 Pages |
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.
Related Topics
Life Sciences
Biochemistry, Genetics and Molecular Biology
Cell Biology
Authors
Xiaohua Peng, Zhilei Cui, Wen Gu, Weiguo Xu, Xuejun Guo,