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Published 18 July 2005. doi:10.1083/jcb.200501164
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 170, Number 2, 285-294
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Article

 Src-like adaptor protein down-regulates T cell receptor (TCR)–CD3 expression by targeting TCR{zeta} for degradation

Margaret D. Myers1,2,4, Leonard L. Dragone3,4, and Arthur Weiss1,2,4

1 Department of Medicine, Rosalind Russell Medical Research Center for Arthritis
2 Department of Microbiology and Immunology, Rosalind Russell Medical Research Center for Arthritis
3 Division of Pediatric Immunology/Rheumatology, Department of Pediatrics
4 Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143

Correspondence to Arthur Weiss: aweiss{at}medicine.ucsf.edu

Src-like adaptor protein (SLAP) down-regulates expression of the T cell receptor (TCR)–CD3 complex during a specific stage of thymocyte development when the TCR repertoire is selected. Consequently, SLAP–/– thymocytes display alterations in thymocyte development. Here, we have studied the mechanism of SLAP function. We demonstrate that SLAP-deficient thymocytes have increased TCR{zeta} chain expression as a result of a defect in TCR{zeta} degradation. Failure to degrade TCR{zeta} leads to an increased pool of fully assembled TCR–CD3 complexes that are capable of recycling back to the cell surface. We also provide evidence that SLAP functions in a pathway that requires the phosphorylated TCR{zeta} chain and the Src family kinase Lck, but not ZAP-70 ({zeta}-associated protein of 70 kD). These studies reveal a unique mechanism by which SLAP contributes to the regulation of TCR expression during a distinct stage of thymocyte development.

Abbreviations used in this paper: DP, double-positive; MFI, mean fluorescence intensity; MHC, major histocompatibility complex; PE, phycoerythrin; RIPA, radioimmunoprecipitation; SH, Src homology; SLAP, Src-like adaptor protein; SP, single-positive; TCR, T cell receptor; WT, wild-type.


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