The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
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© The Rockefeller University Press, 0022-1007/1997/12/2069/ $5.00
The Journal of Experimental Medicine, Volume 186, Number 12, December 15, 1997 2069-2073

Brief Definitive Reports

Itk and Fyn Make Independent Contributions to T Cell Activation

X. Charlene Liao*, Dan R. Littman{ddagger}, and Arthur Weiss*

From the * Department of Microbiology and Immunology, and Department of Medicine, Howard Hughes Medical Institute, University of California, San Francisco, California 94143; and {ddagger} The Skirball Institute of Biomolecular Medicine, Howard Hughes Medical Institute, New York University Medical Center, New York, New York 10016

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.

Address correspondence to Dr. Arthur Weiss, UCSF, Box 0724, 3rd and Parnassus, San Francisco, CA 94143. Phone: 415-476-1291; FAX: 415-502-5081; email: aweiss{at}itsa.ucsf.edu

X.C. Liao is supported by the Cancer Research Fund of the Damon Runyon–Walter Winchell Foundation (1992–1995) and by a Special Fellowship from the Leukemia Society of America, Inc. (1995–1996). D.R. Littman and A. Weiss are investigators of the Howard Hughes Medical Institute.


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