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Molecular and Cellular Biology, August 2007, p. 5275-5285, Vol. 27, No. 15
0270-7306/07/$08.00+0     doi:10.1128/MCB.01967-05
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Aberrant Regulation of Hematopoiesis by T Cells in BAZF-Deficient Mice{triangledown}

Hal E. Broxmeyer,1,{dagger} Sarita Sehra,1,{dagger} Scott Cooper,1 Lisa M. Toney,1 Saritha Kusam,1 Jim J. Aloor,2 Christophe C. Marchal,2 Mary C. Dinauer,2 and Alexander L. Dent1*

Department of Microbiology and Immunology and The Walther Oncology Center, Indiana University School of Medicine, Indianapolis, Indiana 46202, and Walther Cancer Institute, Indianapolis, Indiana 46208,1 Department of Pediatrics and Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana 462022

Received 7 October 2005/ Returned for modification 7 December 2005/ Accepted 16 May 2007

The BAZF (BCL-6b) protein is highly similar to the BCL-6 transcriptional repressor. While BCL-6 has been characterized extensively, relatively little is known about the normal function of BAZF. In order to understand the physiological role of BAZF, we created BAZF-deficient mice. Unlike BCL-6-deficient mice, BAZF-deficient mice are healthy and normal in size. However, BAZF-deficient mice have a hematopoietic progenitor phenotype that is almost identical to that of BCL-6-deficient mice. Compared to wild-type mice, both BAZF-deficient and BCL-6-deficient mice have greatly reduced numbers of cycling hematopoietic progenitor cells (HPC) in the BM and greatly increased numbers of cycling HPC in the spleen. In contrast to HPC from wild-type mice, HPC from BAZF-deficient and BCL-6-deficient mice are resistant to chemokine-induced myelosuppression and do not show a synergistic growth response to granulocyte-macrophage colony-stimulating factor plus stem cell factor. Depletion of CD8 T cells in BAZF-deficient mice reverses several of the hematopoietic defects in these mice. Since both BAZF- and BCL-6-deficient mice have defects in CD8 T-cell differentiation, we hypothesize that both BCL-6 and BAZF regulate HPC homeostasis by an indirect pathway involving CD8 T cells.

* Corresponding author. Mailing address: Department of Microbiology and Immunology and The Walther Oncology Center, 950 W. Walnut St. R2 302, Indiana University School of Medicine, Indianapolis, IN 46202. Phone: (317) 274-7524. Fax: (317) 274-7592. E-mail: adent2{at}iupui.edu

{triangledown} Published ahead of print on 25 May 2007.

{dagger} These two authors contributed equally to this work.

Molecular and Cellular Biology, August 2007, p. 5275-5285, Vol. 27, No. 15
0270-7306/07/$08.00+0     doi:10.1128/MCB.01967-05
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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