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International Immunology, Vol. 15, No. 2, pp. 215-221, February 2003
© 2003 Japanese Society for Immunology

Essential role for Vav1 in activation, but not development, of {gamma}{delta} T cells

Wojciech Swat1,3,6, Ramnik Xavier4, Atsushi Mizoguchi4, Emiko Mizoguchi4, Jessica Fredericks1, Keiko Fujikawa1, Atul K. Bhan4 and Frederick W. Alt1,3,5

1 The Center for Blood Research, 2 Howard Hughes Medical Institute, 3 Department of Pediatrics, The Children’s Hospital, 4 Department of Pathology, Medicine and Molecular Biology, Massachusetts General Hospital, and 5 Department of Genetics, Harvard Medical School, Boston, MA 02115, USA 6 Present address: Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO 63110, USA

Correspondence to: F. W. Alt, The Children’s Hospital, Howard Hughes Medical Institute, 320 Longwood Avenue, Boston, MA 02115, USA; E-mail: alt{at}rascal.med.harvard.edu
Transmitting editor: K. M. Murphy

Vav1 is a guanine nucleotide exchange factor essential in the development and function of {alpha}ß lineage T cells. Here we report that in contrast to profound effects on pre-TCR- or {alpha}ß TCR-dependent events in thymocyte development, Vav1 deficiency has no detectable effect on the development of {gamma}{delta} T cells. Strikingly, however, these {gamma}{delta} T cells are markedly deficient in signaling through the {gamma}{delta} TCR, as evidenced by a lack of proliferation and cytokine production in response to stimulation with anti-{gamma}{delta} TCR antibodies. We propose that Vav1 has a unique and non-redundant role in the initiation of signaling downstream of the {gamma}{delta} TCR in lymphocytes.

Keywords: antigen receptor, lymphocyte activation, lymphocyte development, intestinal epithelial lymphocyte, Vav1


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