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Dlk1 influences differentiation and function of B lymphocytes.

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.

Pubmed ID: 18513163

Authors

  • Raghunandan R
  • Ruiz-Hidalgo M
  • Jia Y
  • Ettinger R
  • Rudikoff E
  • Riggins P
  • Farnsworth R
  • Tesfaye A
  • Laborda J
  • Bauer SR

Journal

Stem cells and development

Publication Data

June 25, 2008

Associated Grants

None

Mesh Terms

  • Animals
  • Antibody Formation
  • B-Lymphocytes
  • Bone Marrow Cells
  • Cell Differentiation
  • Cell Lineage
  • Gene Targeting
  • Homeostasis
  • Immunoglobulins
  • Intercellular Signaling Peptides and Proteins
  • Lymphocyte Subsets
  • Mice
  • Spleen
  • Stem Cells
  • T-Lymphocytes