The Journal of Experimental Medicine
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Published online 4 June 2001.
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© The Rockefeller University Press, 0022-1007/2001/6/1269/ $5.00
The Journal of Experimental Medicine, Volume 193, Number 11, June 4, 2001 1269-1284

Original Article

The Transmembrane Adaptor Protein Trim Regulates T Cell Receptor (Tcr) Expression and Tcr-Mediated Signaling via an Association with the Tcr {zeta} Chain

Henning Kirchgessnera, Jes Dietrichb, Jeanette Scherera, Pia Isomäkic, Vladimir Korinekd, Ivan Hilgertd, Eddy Bruynsa, Albrecht Leoa, Andrew P. Copec, and Burkhart Schravena,e

a Institute for Immunology, Ruprecht-Karls University Heidelberg, D-69120 Heidelberg, Germany
b Institute of Medical Microbiology and Immunology, University of Copenhagen, DK-2200 Copenhagen, Denmark
c Kennedy Institute of Rheumatology Division, Imperial College School of Medicine,
d Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, 14220 Praque, Czech Republic
e Institute for Immunology, Otto-von-Guericke-University Magdeburg, 39120 Magdeburg, Germany
Institute for Immunology, Otto-von-Guericke-University Magdeburg, Leipziger Strasse 44, 39120 Magdeburg, Germany.391-67-15852391-67-15800

burkhart.schraven{at}medizin.uni-magdeburg.de

T cell receptor (TCR)-interacting molecule (TRIM) is a recently identified transmembrane adaptor protein, which is exclusively expressed in T cells. Here we demonstrate that in mature T cells, TRIM preferentially interacts with the TCR via the TCR-{zeta} chains and to a lesser extent via the CD3-{varepsilon}/{gamma} heterodimer. Transient or stable overexpression of TRIM in Jurkat T cells results in enhancement of TCR expression on the cell surface and elevated induction of Ca2+ mobilization after T cell activation. TRIM-mediated upregulation of TCR expression results from inhibition of spontaneous TCR internalization and stabilization of TCR complexes on the cell surface. Collectively, our data identify TRIM as a novel integral component of the TCR complex and suggest that one function of TRIM might be to modulate the strength of signals transduced through the TCR through regulation of TCR expression on the cell surface.

Key Words: T lymphocytes • signal transduction • T cell receptor complex • {zeta} chains • transmembrane adaptor proteins

Abbreviations used in this paper: BFA, brefeldin A; LAT, linker for activation of T cells; SIT, SHP2-interacting transmembrane adaptor protein; SKAP-HOM, Src kinase–associated phosphoprotein homologue; TRIM, TCR-interacting molecule.

© 2001 The Rockefeller University Press


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