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Blood, 1 February 2005, Vol. 105, No. 3, pp. 1288-1294.
Prepublished online as a Blood First Edition Paper on October 12, 2004; DOI 10.1182/blood-2004-04-1453.
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NEOPLASIA
Impaired T- and B-cell development in Tcl1-deficient mice
Sang-Moo Kang,
Maria Grazia Narducci,
Cristina Lazzeri,
Adriana M. Mongiovì,
Elisabetta Caprini,
Antonella Bresin,
Fabio Martelli,
Jay Rothstein,
Carlo Maria Croce,
Max D. Cooper, and
Giandomenico Russo
From the University of Alabama at Birmingham and the Howard Hughes Medical Institute, Birmingham, AL; Istituto Dermopatico dell'Immacolata-Istituto di Ricovero e Cura a Carattere Scientifico, Roma, Italy; and the Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA.
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-CD3 –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.
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