Blood Journal
Leading the way in experimental and clinical research in hematology

Identification of Flt3+CD150- myeloid progenitors in adult mouse bone marrow that harbor T lymphoid developmental potential

  1. Anthony W.S. Chi1,
  2. Alejandro Chavez1,
  3. Lanwei Xu2,
  4. Brittany N. Weber1,
  5. Olga Shestova1,
  6. Andras Shaffer1,
  7. Gerald Wertheim1,
  8. Warren S. Pear1,
  9. David Izon3, and
  10. Avinash Bhandoola1,*
  1. 1 Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA, United States;
  2. 2 Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA, United States;
  3. 3 The Haematology and Leukaemia Division, St Vincent's Institute, Melbourne, VIC, Australia
  1. * Corresponding author; email: bhandooa{at}


Common myeloid progenitors (CMPs) were first identified as progenitors that were restricted to myeloid and erythroid lineages. However, it was recently demonstrated that expression of both lymphoid- and myeloid-related genes could be detected in myeloid progenitors. Furthermore, these progenitors were able to give rise to T and B lymphocytes, in addition to myeloid cells. Yet, it wasn't known whether these progenitors were multipotent at the clonogenic level or there existed heterogeneity within these progenitors with different lineage potential. Here we report that previously defined CMPs possess T lineage potential, and that this is exclusively found in the Flt3+CD150- subset of CMPs at the clonal level. In contrast, we did not detect B lineage potential in CMP subsets. Therefore, these Flt3+CD150- myeloid progenitors were T/myeloid potent. Yet, Flt3+CD150- myeloid progenitors are not likely to efficiently traffic to the thymus and contribute to thymopoiesis under normal conditions due to the lack of CCR7 and CCR9 expression. Interestingly, both Flt3+CD150- and Flt3-CD150- myeloid progenitors are susceptible to Notch1-mediated T-cell acute lymphoblastic leukemia (T-ALL). Hence gain-of-function Notch1 mutations occurring in developing myeloid progenitors, in addition to known T lineage progenitors, could lead to T-ALL oncogenesis.

  • Submitted September 29, 2010.
  • Accepted June 28, 2011.