作者: Adam P. Kohm , Afsaneh Mozaffarian , Virginia M. Sanders
DOI: 10.4049/JIMMUNOL.168.12.6314
关键词: Protein kinase A 、 Molecular biology 、 Neurotransmitter receptor 、 CD86 、 Tyrosine kinase 、 Tropomyosin receptor kinase B 、 breakpoint cluster region 、 B cell 、 Cell biology 、 B-cell receptor 、 Biology
摘要: The costimulatory molecule B7-2 (CD86) is expressed on the surface of APCs, including B cells. Considering importance in regulating both T and cell function, it may be important to understand regulatory mechanisms governing its expression. We report this study that stimulation receptor (BCR) and/or a neurotransmitter receptor, β 2 -adrenergic (β AR), cooperate regulate cell-associated expression vitro vivo. AR further enhanced level BCR-induced cells potentially via protein tyrosine kinase-, kinase A-, C-, mitogen-activated kinase-dependent mechanisms. Importantly, BCR stimulation, but not histone hyperacetylation DNA hypomethylation alone, increased by increasing mRNA stability, NF-κB nuclear binding, NF-κB-dependent gene transcription. Thus, provides additional insight into signaling intermediates molecular which