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The BCL11AXL transcription factor: its distribution in normal and malignant tissues and use as a marker for plasmacytoid dendritic cells

Leukemia volume 20, pages 1439–1441 (2006)Cite this article

The B-cell lymphoma/leukemia 11A (BCL11A) gene was first identified in the rare t(2;14)(p16;q32.3) translocation in aggressive B-cell chronic lymphocytic leukemia and, together with REL, is a candidate for the 2p16 chromosomal amplifications in B-cell malignancies.1 BCL11A encodes a Krüppel zinc-finger transcription factor, and Evi9/Bcl11a/Ctip1 (mouse homologue of human BCL11A) has been shown to be essential for pre-B-cell development and thymocyte maturation.2 There is evidence that Bcl11a, and hence human BCL11A, may not only encode a dominant proto-oncogene but also function as a non-autonomous T-cell tumor suppressor gene.2 Alternative RNA splicing generates at least three BCL11A transcripts with restricted expression in bone marrow, lymphoid tissue and brain. BCL11AXL mRNA is the largest and the most abundant transcript.1

BCL11AXL protein was detected in the nuclei of cells in the mantle zone, the majority of nuclei in the germinal centers and a subpopulation of cells in the interfollicular areas of tonsil and lymph node (Figure 1c). Nuclear staining of the splenic marginal zone was also observed. Double immunolabeling studies demonstrated most of the BCL11AXL-positive cells in the tonsil to be of B-cell origin (Figure 1d), whereas T cells (Figure 1e) and plasma cells (Figure 1f) were BCL11AXL-negative. Only rare BCL11AXL-positive cells were observed in the bone marrow and fetal thymus and these coexpressed either CD68 or CD79a antigen. Although high levels of BCL11A transcripts have been described in peripheral blood B cells (http://symatlas.gnf.org/), BCL11AXL protein expression was not detected in peripheral blood smears or purified CD20-positive B cells from normal subjects. Activation of purified CD20-positive B cells with Staphyloccus aureus and rIL-2 did, however, result in the induction of nuclear expression of BCL11AXL.

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Acknowledgements

This work was supported by grants from the Leukemia Research Fund (KP, AHB, LL, MJ, SA and DYM), the NIH (Grant CA92318 GCI, HL and PWT) and the Medical Research Council (MJSD).

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Authors and Affiliations

  1. Nuffield Department of Clinical Laboratory Sciences, John Radcliffe Hospital, University of Oxford, Oxford, UK

    K Pulford, A H Banham, L Lyne, M Jones, S Ashe, L Stockwin & D Y Mason

  2. Molecular Genetics and Microbiology, University of Texas, Austin, TX, USA

    G C Ippolito, H Liu & P W Tucker

  3. Monoclonal Antibodies Unit, Centro Nacional de Investigaciones Oncologicas, Madrid, Spain

    G Roncador & E Lucas

  4. MRC Toxicology Unit, University of Leicester, Leicester, UK

    R Walewska, L Karran & M J S Dyer

  5. Pathology and Laboratory Medicine, British Columbia Cancer Agency and University of British Columbia, Vancouver, Canada

    R D Gascoyne

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Correspondence to K Pulford.

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Pulford, K., Banham, A., Lyne, L. et al. The BCL11AXL transcription factor: its distribution in normal and malignant tissues and use as a marker for plasmacytoid dendritic cells. Leukemia 20, 1439–1441 (2006). https://doi.org/10.1038/sj.leu.2404260

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