| First Author | Braunstein M | Year | 2010 |
| Journal | Int Immunol | Volume | 22 |
| Issue | 12 | Pages | 963-72 |
| PubMed ID | 21115673 | Mgi Jnum | J:167226 |
| Mgi Id | MGI:4867582 | Doi | 10.1093/intimm/dxq450 |
| Citation | Braunstein M, et al. (2010) HEBAlt enhances the T-cell potential of fetal myeloid-biased precursors. Int Immunol 22(12):963-72 |
| abstractText | Hematopoiesis is controlled by the interplay between transcription factors and environmental signals. One of the primary determinants of the T-lineage choice is Delta-like (DL)-Notch signaling, which promotes T-cell development and inhibits B-cell development. We have found that the transcription factor HEBAlt is up-regulated in early hematopoietic precursors in response to DL-Notch signaling and that it can promote early T-cell development. Here, we identified a population of lineage-negative Sca-1c-kit(+) (LK) cells in the mouse fetal liver that rapidly gave rise to myeloid cells and B cells but exhibited very little T-cell potential. However, forced expression of HEBAlt in these precursors restored their ability to develop into T cells. We also showed that Ikaros and Notch1 are up-regulated in response to HEBAlt over-expression and that activated Notch1 enhances the ability of LK cells to enter the T-cell lineage. Furthermore, the myeloid transcription factor C/EBPalpha is down-regulated in response to HEBAlt. We therefore propose that HEBAlt plays a role in the network that enforces the T-lineage fate and limits myeloid fate during hematopoiesis. |
