Open AccessDisruption of epithelial gamma delta T cell repertoires by mutation of the Syk tyrosine kinase.
Author(s) -
Caroline A. Mallick-Wood,
William Pao,
Alec M. Cheng,
Julia M. Lewis,
Surendra U. Kulkarni,
Joseph B. Bolen,
Bruce Rowley,
Robert E. Tigelaar,
Tony Pawson,
Adrian Hayday
Publication year - 1996
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.93.18.9704
Subject(s) - syk , tyrosine kinase , biology , gamma delta t cell , microbiology and biotechnology , cancer research , t cell , t cell receptor , signal transduction , immunology , immune system
Chimeric mice in which lymphocytes are deficient in the Syk tyrosine kinase have been created. Compared with Syk-positive controls, mice with Syk -/- lymphocytes display substantial depletion of intraepithelial gamma delta T cells in the skin and gut, with developmental arrest occurring after antigen receptor gene rearrangement. In this dependence on Syk, subsets of intraepithelial gamma delta T cells are similar to B cells, but distinct from splenic gamma delta T cells that develop and expand in Syk-deficient mice. The characteristic associations of certain T-cell receptor V gamma/V delta gene rearrangements with specific epithelia are also disrupted by Syk deficiency.