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Science 23 April 1999:
Vol. 284. no. 5414, pp. 638 - 641
DOI: 10.1126/science.284.5414.638
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Reports

Requirement for Tec Kinases Rlk and Itk in T Cell Receptor Signaling and Immunity

Edward M. Schaeffer, 1* Jayanta Debnath, 12*dagger George Yap, 3 Daniel McVicar, 2 X. Charlene Liao, 4 Dan R. Littman, 5 Alan Sher, 3 Harold E. Varmus, 2 Michael J. Lenardo, 3 Pamela L. Schwartzberg 12ddagger

T cell receptor (TCR) signaling requires activation of Zap-70 and Src family tyrosine kinases, but requirements for other tyrosine kinases are less clear. Combined deletion in mice of two Tec kinases, Rlk and Itk, caused marked defects in TCR responses including proliferation, cytokine production, and apoptosis in vitro and adaptive immune responses to Toxoplasma gondii in vivo. Molecular events immediately downstream from the TCR were intact in rlk-/-itk-/- cells, but intermediate events including inositol trisphosphate production, calcium mobilization, and mitogen-activated protein kinase activation were impaired, establishing Tec kinases as critical regulators of TCR signaling required for phospholipase C-gamma activation.

1 National Human Genome Research Institute,
2 National Cancer Institute,
3 National Institute for Allergy and Infectious Diseases, NIH, Bethesda, MD 20892, USA.
4 Tularik, 2 Corporate Drive, South San Francisco, CA 94080, USA.
5 Skirball Institute of Biomolecular Medicine, NYU Medical Center, 540 First Avenue, New York, NY 10016, USA.
*   These authors contributed equally to this work.

dagger    Present address: Department of Pathology, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115, USA.

ddagger    To whom correspondence should be addressed. E-mail: pams{at}nhgri.nih.gov

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