| First Author | Raghunandan R | Year | 2008 |
| Journal | Stem Cells Dev | Volume | 17 |
| Issue | 3 | Pages | 495-507 |
| PubMed ID | 18513163 | Mgi Jnum | J:145076 |
| Mgi Id | MGI:3833481 | Doi | 10.1089/scd.2007.0102 |
| Citation | Raghunandan R, et al. (2008) Dlk1 influences differentiation and function of B lymphocytes. Stem Cells Dev 17(3):495-507 |
| abstractText | The Dlk1 (delta-like-1) gene is a member of the epidermal growth factor (EGF)-like homeotic gene family. It influences cell-cell interactions between stromal cells and pro-B cells in vitro. To define the in vivo role of the dlk protein in B cell development, we established a Dlk1-/- mouse model. In spleens of Dlk1-/- mice, transitional B cell numbers were increased and the ratio between transitional B cell subsets was altered. Numbers of follicular B cells decreased, while the number of marginal zone B cells and the size of the marginal zone were increased. Loss of dlk resulted in increased immunoglobulin G1 (IgG1) and IgG3 in preimmune sera. Furthermore, there was an exaggerated primary T-dependent antigen-specific humoral immune response. In bone marrow, the lack of dlk led to increased numbers of the earliest B lineage cells in young mice without affecting numbers of later B lineage cells. In vitro experiments showed that lack of dlk on either stromal cells or pro-B cells caused changes in differentiation and proliferation of pro-B cells, suggesting that lack of dlk leads to changes in cell-cell interactions in the bone marrow microenvironment. These results show that dlk expression is essential for normal B cell development. |
