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 Blood, 15 October 2006, Vol. 108, No. 8, pp. 2695-2702.
Prepublished online as a Blood First Edition Paper on June 29, 2006; DOI 10.1182/blood-2006-05-021790.

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IMMUNOBIOLOGY

BCL11B participates in the activation of IL2 gene expression in CD4+ T lymphocytes

Valeriu B. Cismasiu, Sailaja Ghanta, Javier Duque, Diana I. Albu, Hong-Mei Chen, Rohini Kasturi, and Dorina Avram

From the Center for Cell Biology and Cancer Research, Albany Medical College, Albany, NY.

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 the interleukin-2 (IL2) gene expression following activation through T-cell receptor (TCR). BCL11B augments expression from the IL2 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.


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