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*
Department of Pediatric Oncology, Dana-Farber Cancer Institute, and Department of Pediatrics, Harvard Medical School, Boston, MA 02115;
Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720;
Department of Microbiology and Immunology, University of California, San Francisco, CA 94143; and
§
Howard Hughes Medical Institute, Skirball Institute of Biomolecular Medicine, New York University Medical Center, New York, NY 10016
Previous studies have shown that CD8ß plays a role in both
enhancing CD8
-associated Lck kinase activity and promoting the
development of CD8-lineage T cells. To examine the role of this
enhancement in the maturation of CD8-lineage cells, we assessed
CD8-associated Lck kinase activity in both T cell hybridomas and
thymocytes of mice expressing CD8ß mutations known to impair CD8 T
cell development. Lack of CD8ß expression or expression of a
cytoplasmic domain-deleted CD8ß resulted in a severalfold reduction
in CD8-associated Lck kinase activity compared with that observed
with cells expressing wild-type CD8ß chain. This analysis indicated a
critical role for the cytoplasmic domain of CD8ß in the regulation of
CD8-associated Lck activity. Decreased CD8-associated Lck
activity observed with the various CD8ß mutations also correlated
with diminished in vivo cellular tyrosine phosphorylation. In addition,
analysis of CD8ß mutant mice (CD8ß-/- or
cytoplasmic domain-deleted CD8ß transgenic) indicated that the degree
of reduction in CD8-associated Lck activity associated with each
mutation correlated with the severity of developmental impairment.
These results support the importance of CD8ß-mediated enhancement of
CD8-associated Lck kinase activity in the differentiation of CD8
single-positive thymocytes.
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