脱颗粒
细胞因子
STAT1
白细胞介素33
p38丝裂原活化蛋白激酶
信号转导
肥大细胞
细胞生物学
酪氨酸激酶
分子生物学
生物
化学
MAPK/ERK通路
免疫学
白细胞介素
生物化学
受体
作者
Jung Youn Seo,Dae Yong Kim,Yun Song Lee,Jai Youl Ro
出处
期刊:Cytokine
[Elsevier]
日期:2009-04-01
卷期号:46 (1): 51-60
被引量:17
标识
DOI:10.1016/j.cyto.2008.12.008
摘要
IFNγ is strongly related to mast cell-associated diseases. There are many reports that IFNγ inhibits mast cell degranulation. However, inflammatory cytokine production in mast cells stimulated with IFNγ has not yet been clearly investigated. Therefore, we aimed to investigate the signaling pathways of cytokine production in mast cells stimulated with IFNγ. Human mast cell line (HMC)-1 or mouse bone marrow-derived mast cells (BMMCs) were stimulated with IFNγ (100 units) for time periods indicated. Expressions of proteins and mRNAs of cytokines were determined by ELISA and RT-PCR, respectively, activities of MAP kinases, PKC, JAK1/2, and STAT1 on tyrosine 701 and serine 727 by immunoblotting, the DNA-binding activity of the transcription factors by electrophoretic mobility shift assay. IFNγ-stimulated mast cells showed increase in expressions of proteins and mRNAs of inflammatory cytokines, phosphorylations of MAP kinases, PKCα and βI, JAK1/2, and STAT1 on tyrosine 701 and serine 727. JAK inhibitor or PKC inhibitors inhibited the phosphorylations of p38 kinase, STAT1 on serine 727, and activities of NF-κB and AP-1 compared to IFNγ stimulation alone. These data suggest that IFNγ-stimulated mast cells induce productions of inflammatory cytokines through PKC/p38/NF-κB and AP-1 pathways, not through classical JAK/STAT1 pathway, in both mast cells.
科研通智能强力驱动
Strongly Powered by AbleSci AI