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Departments of
*
Immunology and
Anatomy and
PRESTO Research Project, Institute of Basic Medical Sciences, and
§
Center for TARA, University of Tsukuba, Tsukuba, Japan; and
¶
Division of Immunology, Beth Israel Hospital, Harvard Medical School, Boston, MA 02215
Transgenic mice with human CD3
gene have been shown to exhibit
early arrest of T cell development in the thymus. The present study
shows that, instead of T cells, B cells are generated in the thymus of
a line, tg26, of the human CD3 transgenic mice. The accumulation
of mature B cells in the thymus was found only in tg26 mice, not in
other human CD3 transgenic mouse lines or other T cell-deficient
mice, including CD3- knockout mice and TCR-ß/TCR-
double
knockout mice. Hanging drop-mediated transfer into
2-deoxyguanosine-treated thymus lobes showed that lymphoid progenitor
cells rather than thymus stromal cells were responsible for abnormal B
cell development in tg26 thymus, and that tg26 fetal liver cells
were destined to become B cells in normal thymus even in the presence
of normal progenitor cells undergoing T cell development. These results
indicate that lymphoid progenitor cells in tg26 mice are genetically
defective in thymic choice between T cells and B cells, generating B
cells even in normal thymus environment. Interestingly, tg26
thymocytes expressed GATA-3 and TCF-1, but not LEF-1 and PEBP-2
,
among T cell-specific transcription factors that are involved in early
T cell development, indicating that GATA-3 and TCF-1 expressed during
thymocyte development do not necessarily determine the cell fate into T
cell lineage. Thus, tg26 mice provide a novel mouse model in that
lineage choice between T and B lymphocytes is genetically
defective.
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