The transmembrane adaptor protein TRIM regulates T cell receptor (TCR) expression and TCR-mediated signaling via an association with the TCR zeta chain

• Published in: The Journal of experimental medicine Vol. 193; no. 11; pp. 1269 - 1284
• Main Authors: Kirchgessner, H, Dietrich, J, Scherer, J, Isomäki, P, Korinek, V, Hilgert, I, Bruyns, E, Leo, A, Cope, A P, Schraven, B
• Format: Journal Article
• Language: English
• Published: United States The Rockefeller University Press 04-06-2001
• Subjects: Adaptor Proteins, Signal Transducing; Amino Acid Sequence; Animals; Calcium - metabolism; Carrier Proteins - physiology; COS Cells; Dimerization; Humans; Jurkat Cells; Membrane Proteins - chemistry; Membrane Proteins - physiology; Molecular Sequence Data; Original; Receptors, Antigen, T-Cell - chemistry; Receptors, Antigen, T-Cell - physiology; Signal Transduction
• ISSN: 0022-1007; 1540-9538
• DOI: 10.1084/jem.193.11.1269

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-straightepsilon/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 Ca(2+) 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.