International Immunology, Vol. 14, No. 9, pp. 1039-1053,
September 2002
© 2002 Japanese Society for Immunology
A mouse strain defective for 
ß versus 
T cell lineage commitment
1 Department of Biology and Cancer Center, 2 The Howard Hughes Medical Institute, and 3 Department of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, CA 92093, USA 4 Celltech Chiroscience R & D, Bothell, WA 98021, USA 5 Present address: Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115, USA
Correspondence to: S. M. Hendrick; E-mail: shedrick{at}ucsd.edu
Transmitting editor: M. J. Bevan
As a result of a transgene insertion and chromosomal deletion, a mutant mouse strain has been found that is defective in the lineage commitment step that produces a balance of 
ß and 
T cells. The mice produce a reduced population of ß CD4 T cells and almost no ß CD8 T cells. Within the CD4 and CD8 populations in the thymus there exist abnormal subsets that express the TCR. These TCR-expressing cells populate the peripheral lymphoid organs such that up to 75% of the CD8 T cells in the lymph nodes and spleen express a TCR. Further analyses indicate that the regulation that prevents dual TCR expression has been impaired. The locus of insertion and deletion was mapped to chromosome 10 26 cM. We have analyzed the entire locus and, in addition, the gene expression changes in early thymocytes were analyzed by gene array technology. The analysis of this mutant strain indicates that the ß versus lineage decision can be profoundly disregulated independently of successful gene rearrangements.
Keywords: chromosomal deletion, development, immune response, lineage commitment, T cells
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