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  • Title: Expression of the p56(Lck) Y505F mutation in CD45-deficient mice rescues thymocyte development.
    Author: Seavitt JR, White LS, Murphy KM, Loh DY, Perlmutter RM, Thomas ML.
    Journal: Mol Cell Biol; 1999 Jun; 19(6):4200-8. PubMed ID: 10330160.
    Abstract:
    Mice deficient in the transmembrane protein tyrosine phosphatase CD45 exhibit a block in thymocyte development. To determine whether the block in thymocyte development was due to the inability to dephosphorylate the inhibitory phosphorylation site (Y505) in p56(lck) (Lck), we generated CD45-deficient mice that express transgenes for the Lck Y505F mutation and the DO11.10 T-cell antigen receptor (TCR). CD4 single-positive T cells developed and accumulated in the periphery. Treatment with antigen resulted in thymocyte apoptosis and the loss of transgenic-TCR-bearing cells. Peripheral CD45-deficient T cells from the mice expressing both transgenes responded to antigen by increasing CD69 expression, interleukin-2 production, and proliferation. These results indicate that thymocyte development requires the dephosphorylation of the inhibitory site in Lck by CD45.
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