| First Author | Cooper CL | Year | 2012 |
| Journal | Blood | Volume | 119 |
| Issue | 23 | Pages | 5438-48 |
| PubMed ID | 22517907 | Mgi Jnum | J:188661 |
| Mgi Id | MGI:5441406 | Doi | 10.1182/blood-2011-12-397976 |
| Citation | Cooper CL, et al. (2012) Non-cell-autonomous hedgehog signaling promotes murine B lymphopoiesis from hematopoietic progenitors. Blood 119(23):5438-48 |
| abstractText | The role of hedgehog (Hh) signaling in B lymphopoiesis has remained unclear. We observed that the proliferation of pro-B cells in stromal cocultures was impaired by interruption of Hh signaling, prompting us to investigate whether the target of Hh antagonism was intrinsic or extrinsic to the B-lymphoid compartment. In the present study, using conditional deletion of the pathway activator gene Smo, we found that cell-autonomous Hh signaling is dispensable for B-cell development, B-lymphoid repopulation of the BM, and humoral immune function. In contrast, depletion of the Smo protein from stromal cells was associated with impaired generation of B-lymphoid cells from hematopoietic stem progenitor cells, whereas reciprocal removal of Smo from these cells had no effect on the production of B-cell progenitors. Depletion of Smo from stromal cells was associated with coordinate down-regulation of genes for which expression is associated with osteoblastoid identity and B-lymphopoietic activity. The results of the present study suggest that activity of the Hh pathway within stromal cells promotes B lymphopoiesis in a non-cell-autonomous fashion. |
