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.
journal_name
Mol Cell Bioljournal_title
Molecular and cellular biologyauthors
Seavitt JR,White LS,Murphy KM,Loh DY,Perlmutter RM,Thomas MLdoi
10.1128/mcb.19.6.4200subject
Has Abstractpub_date
1999-06-01 00:00:00pages
4200-8issue
6eissn
0270-7306issn
1098-5549journal_volume
19pub_type
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