BCL11B Upregulates the Expression of RelA in T Cells Stimulated with Staphylococcal Enterotoxin A

被引:0
作者
Y. Yan
S. Wang
C. Lin
机构
[1] Southern Medical University,State Key Laboratory for Organ Failure Research & National Clinical Research Center for Kidney Disease, Guangdong Provincial Clinical Research Center for Kidney Disease, Division of Nephrology, Nanfang Hospital
[2] Maternity and Child Health Hospital of Anhui Province,Affiliated Maternity and Child Health Hospital of Anhui Medical University
[3] Jinan University,Department of Microbiology and Immunology
来源
Bulletin of Experimental Biology and Medicine | 2022年 / 174卷
关键词
BCL11B; RelA; staphylococcal enterotoxin A; T cell; leukemia;
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摘要
We explored the potential link between RelA and BCL11B transcription factors. To this end, Jurkat and Raji cells (Jurkat:Raji 10:1), as well as normal human peripheral blood T cells, were activated by staphylococcal enterotoxin A (SEA) and the expressions of both BCL11B and RelA mRNA and proteins were detected. BCL11B small interfering RNA was then transduced into Jurkat cells. Under the effect of SEA stimulation, the expression of BCL11B and RelA mRNA increased in two types of T cell lines over time, and the results were comparable with the levels of expression of BCL11B and RelA proteins. In the BCL11B-knockdown cells, the expression of RelA protein did not increase. These findings suggest that BCL11B regulates RelA expression in Jurkat cells and human peripheral blood T cells from healthy donors via the T-cell receptor signaling pathway.
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页码:259 / 264
页数:5
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