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J. Exp. Med.,
Volume 188, Number 9, November 2, 1998 1575-1586
/
from CD3 Signaling
By
From the * Department of Microbiology and Immunology, McGill University, Montreal, Quebec,
Canada H3A 2B4; the T cell activation and clonal expansion is the result of the coordinated functions of the receptors
for antigen and interleukin (IL)-2. The protein tyrosine kinase p56lck is critical for the generation of signals emanating from the T cell antigen receptor (TCR) and has also been demonstrated to play a role in IL-2 receptor signaling. We demonstrate that an IL-2-dependent, antigen-specific CD4+ T cell clone is not responsive to anti-TCR induced growth when propagated in IL-2, but remains responsive to both antigen and CD3 Department of Immunology, University of Toronto, and The Arthritis and
Immune Disorder Research Center, Toronto, Ontario, Canada M5G 2M9; the § Department of
Microbiology and Immunology, University of Miami School of Medicine, Miami, Florida 33101; the McGill Cancer Centre and the Departments of Biochemistry, Medicine, and Oncology, McGill
University, Montreal, Quebec, Canada H3G 1Y6; and the ¶ Howard Hughes Medical Institute,
University of Chicago, Chicago, Illinois 60637
-specific monoclonal antibody. Survival of this IL-2-dependent clone in the absence of IL-2 was supported by overexpression of exogenous Bcl-xL. Culture of this clonal variant in the absence of IL-2 rendered it
susceptible to anti-TCR-induced signaling, and correlated with the presence of kinase-active
Lck associated with the plasma membrane. The same phenotype is observed in primary, resting
CD4+ T cells. Furthermore, the presence of kinase active Lck associated with the plasma membrane correlates with the presence of ZAP 70-pp21
complexes in both primary T cells and T
cell clones in circumstances of responsive anti-TCR signaling. The results presented demonstrate that IL-2 signal transduction results in the functional uncoupling of the TCR complex
through altering the subcellular distribution of kinase-active Lck.
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