title: The role of BCL11B in regulating the proliferation of human naive T cells.
abstract: 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 Vβ subfamilies was observed. After BCL11B knockdown, a similar distribution of Vβ 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.
authors.affiliation: Institute of Hematology, Medical College, Jinan University, Guangzhou 510632, People's Republic of China.
authors.forename: Si
authors.initials: S
authors.lastname: Chen
authors.forename: Xin
authors.initials: X
authors.lastname: Huang
authors.forename: Shaohua
authors.initials: S
authors.lastname: Chen
authors.forename: Lijian
authors.initials: L
authors.lastname: Yang
authors.forename: Qi
authors.initials: Q
authors.lastname: Shen
authors.forename: Haitao
authors.initials: H
authors.lastname: Zheng
authors.forename: Bo
authors.initials: B
authors.lastname: Li
authors.forename: Piotr
authors.initials: P
authors.lastname: Grabarczyk
authors.forename: Grzegorz K
authors.initials: GK
authors.lastname: Przybylski
authors.forename: Christian A
authors.initials: CA
authors.lastname: Schmidt
authors.forename: Yangqiu
authors.initials: Y
authors.lastname: Li
mesh_terms: D000328:Adult; D053446:CASP8 and FADD-Like Apoptosis Regulating Protein / Q000235:genetics / Q000276:immunology; D053455:Caspase 10 / Q000235:genetics / Q000276:immunology; D053181:Caspase 8 / Q000235:genetics / Q000276:immunology; D049109:Cell Proliferation; D002470:Cell Survival; D002478:Cells, Cultured; D054357:Chemokine CXCL10 / Q000235:genetics / Q000276:immunology; D054371:Chemokine CXCL11 / Q000235:genetics / Q000276:immunology; D015870:Gene Expression / Q000235:genetics / Q000276:immunology*; D020869:Gene Expression Profiling; D055785:Gene Knockdown Techniques; D006801:Humans; D008213:Lymphocyte Activation; D008297:Male; D010957:Plasmids; D034741:RNA, Small Interfering / Q000235:genetics / Q000276:immunology; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000235:genetics / Q000276:immunology; D012097:Repressor Proteins / Q000235:genetics / Q000276:immunology*; D015398:Signal Transduction / Q000235:genetics / Q000276:immunology*; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology* / Q000378:metabolism; D014162:Transfection; D025521:Tumor Suppressor Proteins / Q000235:genetics / Q000276:immunology*
chemical_list: C479740:BCL11B protein, human; D053446:CASP8 and FADD-Like Apoptosis Regulating Protein; C506386:CFLAR protein, human; C114753:CXCL10 protein, human; D054357:Chemokine CXCL10; D054371:Chemokine CXCL11; D034741:RNA, Small Interfering; D016693:Receptors, Antigen, T-Cell, alpha-beta; D012097:Repressor Proteins; D025521:Tumor Suppressor Proteins; C505530:CASP8 protein, human; D053455:Caspase 10; D053181:Caspase 8; C506438:CASP10 protein, human