Abstract
Abstract The BAZF (BCL6b) protein is highly similar to the BCL6 transcriptional repressor. While BCL6 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 BCL6-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 BCL6-deficient mice. Compared to wild-type mice, both BAZF-deficient and BCL6-deficient mice have greatly reduced numbers of cycling hematopoietic progenitor cells (HPC) in the bone marrow and greatly increased numbers of cycling HPC in the spleen. In contrast to HPC from wild-type mice, HPC from BAZF-deficient and BCL6-deficient mice are resistant to chemokine-induced myelo-suppression and do not show a synergistic growth response to GM-CSF 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 BCL6-deficient mice have defects in CD8 T cell differentiation, we hypothesize that both BCL6 and BAZF regulate HPC homeostasis by an indirect pathway involving CD8 T cells.
Published Version
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