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Molecular and Cellular Biology, December 1999, p. 8240-8253, Vol. 19, No. 12
Department of Cell Biology, Kaplan Cancer
Center, New York University School of Medicine, New York, New York
10016
Received 5 February 1999/Returned for modification 23 March
1999/Accepted 23 August 1999
Id1 is an inhibitor of a group of basic helix-loop-helix
transcription factors, collectively called E proteins, which includes E12, E47, E2-2, and HEB. We have generated transgenic mice in which Id1
is specifically expressed in T cells. The total number of thymocytes in
these mice is less than 4% of that in wild-type mice. The majority of
the transgenic thymocytes are CD4 and CD8 double negative and bear the
cell surface markers of multipotent progenitor cells. A small number of
thymocytes, however, differentiate into CD4 or CD8 single-positive T
cells, which also display different characteristics from their
wild-type counterparts. More importantly, apoptotic cells constitute
about 50% of the total thymocytes. These apoptotic thymocytes have
rearranged their T-cell receptor genes, suggesting that they are
differentiating T cells. This finding has raised the possibility that
the T-cell deficiency in Id1 transgenic mice is the result of a massive
apoptosis of differentiating T cells triggered by Id1 expression as
opposed to a developmental block at the earliest progenitor stage. The progenitor cells accumulated in the transgenic mice might have survived
because they are not susceptible to the apoptotic signals. Despite the
massive cell death of the thymocytes at young ages, Id1 transgenic mice
frequently develop T-cell lymphoma later in their life span, and
lymphomagenesis appears to occur at different stages of T-cell
development. Taken together, our data suggest that E proteins, being
the targets of Id1, are essential regulators for normal T-cell
differentiation and tumor suppression.
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Massive Apoptosis of Thymocytes in
T-Cell-Deficient Id1 Transgenic Mice
*
Corresponding author. Present address: Oklahoma Medical
Research Foundation, 825 Northeast 13th St., Oklahoma City, OK 73104. Phone: (405) 271-2864. Fax: (405) 271-7128. E-mail:
XH-Sun{at}omrf.ouhsc.edu.
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