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Disruption of Epithelial γ δ T Cell Repertoires by Mutation of the Syk Tyrosine Kinase

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 γ δ T cells in the skin and gut, with developmental arrest occurring after antigen recept...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 1996-09, Vol.93 (18), p.9704-9709
Main Authors: Mallick-Wood, Caroline A., Pao, William, Cheng, Alec M., Lewis, Julia M., Kulkarni, Sarang, Bolen, Joseph B., Rowley, Bruce, Tigelaar, Robert E., Pawson, Tony, Hayday, Adrian C.
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Language:English
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Summary: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 γ δ T cells in the skin and gut, with developmental arrest occurring after antigen receptor gene rearrangement. In this dependence on Syk, subsets of intraepithelial γ δ T cells are similar to B cells, but distinct from splenic γ δ T cells that develop and expand in Syk-deficient mice. The characteristic associations of certain T-cell receptor Vγ /Vδ gene rearrangements with specific epithelia are also disrupted by Syk deficiency.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.93.18.9704