| First Author | Kang SM | Year | 2005 |
| Journal | Blood | Volume | 105 |
| Issue | 3 | Pages | 1288-94 |
| PubMed ID | 15479728 | Mgi Jnum | J:96607 |
| Mgi Id | MGI:3531035 | Doi | 10.1182/blood-2004-04-1453 |
| Citation | Kang SM, et al. (2005) Impaired T- and B-cell development in Tcl1-deficient mice. Blood 105(3):1288-94 |
| abstractText | TCL1, the overexpression of which may result in T-cell leukemia, is normally expressed in early embryonic tissues, the ovary, and lymphoid lineage cells. Our analysis of mouse B-lineage cells indicates that Tcl1 expression is initiated in pro-B cells and persists in splenic marginal zone and follicular B cells. T-lineage Tcl1 expression begins in thymocyte progenitors, continues in CD4(+)CD8(+) thymocytes, and is extinguished in mature T cells. In Tcl1-deficient mice, we found B lymphopoiesis to be compromised at the pre-B cell stage and T-cell lymphopoiesis to be impaired at the CD4(+)CD8(+) thymocyte stage. A corresponding increase was observed in thymocyte susceptibility to anti-CD3epsilon-induced apoptosis. Reduced numbers of splenic follicular and germinal center B cells were accompanied by impaired production of immunoglobulin G1 (IgG1) and IgG2b antibodies in response to a T-dependent antigen. The marginal zone B cells and T-cell-independent antibody responses were also diminished in Tcl1(-/-) mice. This analysis indicates a significant role for Tcl1, a coactivator of Akt signaling, in normal T- and B-cell development and function. |
