Submitted December 12, 2005
Accepted June 9, 2006
BCL11B participates in the activation of interleukin-2
gene expression in CD4+ T lymphocytes
Valeriu B Cismasiu, Sailaja Ghanta, Javier Duque, Diana Albu, Hong-Mei Chen, Rohini Kasturi, and Dorina Avram*
Center for Cell Biology and Cancer Research, Albany Medical College, Albany, NY, USA
* Corresponding author; email: avramd{at}mail.amc.edu.
BCL11A and BCL11B are transcriptional regulators important for lymphopoiesis and previously associated with hematopoietic malignancies. Ablation of the mouse BCL11B locus results in failure to generate double positive thymocytes, implicating a critical role of BCL11B in T cell development. However, BCL11B is also expressed in CD4+ T lymphocytes, both in resting and activated states. Here we show both in transformed and primary CD4+ T cells that BCL11B participates in the control of interleukin-2 (IL-2) gene expression following activation through T cell receptor (TCR). BCL11B augments expression from IL-2 promoter through direct binding to the US1 site. In addition, BCL11B associates with the p300 coactivator in CD4+ T cells activated through TCR, which may account for its transcriptional activation function. These results provide the first evidence that BCL11B, originally described as a transcriptional repressor, activates transcription of a target gene in the context of T cell activation.
