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J. Exp. Med.,
Volume 186, Number 12, December 15, 1997 2069-2073
By
From the * Department of Microbiology and Immunology, and Department of Medicine, Howard
Hughes Medical Institute, University of California, San Francisco, California 94143; and Itk is a member of the Btk/Tec/Itk family of nonreceptor protein tyrosine kinases (PTKs), and
has been implicated in T cell antigen receptor (TCR) signal transduction. Lck and Fyn are the Src-family nonreceptor PTKs that are involved in TCR signaling. To address the question of
how these members of different families of PTKs functionally contribute to T cell development
and to T cell activation, mice deficient for both Itk and either Lck or Fyn were generated. The
Itk/Lck doubly deficient mice exhibited a phenotype similar to that of Lck-deficient mice. The
phenotype of the Itk/Fyn doubly deficient mice was similar to that of Itk deficient mice. However the Itk/Fyn doubly deficient mice exhibited a more severe defect in TCR-induced proliferation of thymocytes and peripheral T cells than did mice deficient in either kinase alone.
These data support the notion that Itk and Fyn both make independent contributions to TCR-induced T cell activation.
The
Skirball Institute of Biomolecular Medicine, Howard Hughes Medical Institute, New York University
Medical Center, New York, New York 10016
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