The role of BCL11B in regulating the proliferation of human naive T cells

详细信息	查看全文 | 推荐本文 |

• 作者：Si Chen^a ; Xin Huang^a ; Shaohua Chen^a ; Lijian Yang^a ; Qi Shen^a ; Haitao Zheng^a ; Bo Li^a ; Piotr Grabarczyk^b ; Grzegorz K. Przybylski^b ; Christian A. Schmidt^b ; Yangqiu Li^a ; ^c ; ^{yangqiuli@hotmail.com}
• 关键词：BCL11B gene ; Naive T cells ; Small interfering RNA ; Gene expression profiling ; T-cell proliferation
• 刊名：Human Immunology
• 出版年：2012
• 期刊代码：75_01988859
• 类别：bio
• 出版时间：May, 2012
• 卷：73
• 期：5
• 页码：456-464
• 文件大小：2458 K

摘要

The effect of the B-cell chronic lymphocytic leukemia/lymphoma 11B gene (BCL11B) on human T-cell regulation remains unclear. To characterize the functions of BCL11B, recombinant BCL11B and BCL11B siRNA were transfected into human naive T cells to overexpress or knock down BCL11B expression, respectively. After BCL11B overexpression, the proliferation ability and the T-helper (Th) subset were increased, whereas no significant alteration in the expression pattern and clonality of the T-cell receptor V尾 subfamilies was observed. After BCL11B knockdown, a similar distribution of V尾 subfamilies was detected in the naive T cells; however, the proliferation capacity substantially decreased. Global gene expression profiling revealed that the dysregulated genes were mainly involved in T-cell activation and proliferation. BCL11B could selectively promote Th-cell differentiation because of increased CXCL10 and CXCL11 expression. BCL11B suppression may inhibit proliferation and induce apoptosis, which may relate to changes in the expression of CFLAR-CASP8-CASP10 in the mitochondrial pathways. In conclusion, BCL11B is required for T-cell survival; its overexpression could effectively increase the T-cell activation and proliferation abilities and Th-cell differentiation as well.