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Prepublished online as a Blood First Edition Paper on January 30, 2003; DOI 10.1182/blood-2002-10-3139.
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Blood, 1 June 2003, Vol. 101, No. 11, pp. 4342-4346
HEMATOPOIESIS
Pax5 determines B- versus T-cell fate and does not block early myeloid-lineage development
Claudiu V. Cotta,
Zheng Zhang,
Hyung-Gyoon Kim, and
Christopher A. Klug
From the Department of Pathology, University of Alabama at Birmingham, Birmingham; Department of Microbiology, University of Alabama at Birmingham, Birmingham; and the Division of Developmental and Clinical Immunology, University of Alabama at Birmingham, Birmingham.
Progenitor B cells deficient in Pax5 are developmentally multipotent, suggesting that Pax5 is necessary to maintain commitment to the B-cell lineage. Commitment may be mediated, in part, by Pax5 repression of myeloid-specific genes. To determine whether Pax5 expression in multipotential cells is sufficient to restrict development to the B-cell lineage in vivo, we enforced expression of Pax5 in hematopoietic stem cells using a retroviral vector. Peripheral blood analysis of all animals reconstituted with Pax5-expressing cells indicated that more than 90% of Pax5-expressing cells were B220+ mature B cells that were not malignant. Further analysis showed that Pax5 completely blocked T-lineage development in the thymus but did not inhibit myelopoiesis or natural killer (NK) cell development in bone marrow. These results implicate Pax5 as a critical regulator of B- versus T-cell developmental fate and suggest that Pax5 may promote commitment to the B-cell lineage by mechanisms that are independent of myeloid gene repression.
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