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Originally published In Press as doi:10.1074/jbc.M110675200 on April 11, 2002

J. Biol. Chem., Vol. 277, Issue 24, 21123-21129, June 14, 2002
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Regulation of T Cell Receptor CD3zeta Chain Expression by L-Arginine*

Paulo C. RodriguezDagger , Arnold H. ZeaDagger , Kirk S. CulottaDagger , Jovanny ZabaletaDagger , Juan B. Ochoa§, and Augusto C. OchoaDagger

From the Dagger  Tumor Immunology Program, Stanley S. Scott Cancer Center and Department of Pediatrics, Louisiana State University, Health Sciences Center, New Orleans, Louisiana 70112 and the § Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania 15261

L-Arg plays a central role in the normal function of several organ systems including the immune system. L-Arg can be depleted by arginase I produced by macrophages and hepatocytes in several disease states such as trauma and sepsis and following liver transplantation. The decrease in L-Arg levels induces a profound decrease in T cell function through mechanisms that have remained unclear. The data presented here demonstrate that Jurkat T cells cultured in medium without L-Arg (L-Arg-free RPMI) have a rapid decrease in the expression of the T cell antigen receptor zeta  chain (CD3zeta ), the principal signal transduction element in this receptor, and a decrease in T cell proliferation. This phenomenon is completely reversed by the replenishment of L-Arg but not other amino acids. These changes are not caused by cell apoptosis; instead, the diminished expression of CD3zeta protein is paralleled by a decrease in CD3zeta mRNA. This change in CD3zeta mRNA expression is not caused by a decrease in the transcription rate but rather by a significantly shorter CD3zeta mRNA half-life. This mechanism is sensitive to cycloheximide. Therefore, the regulation of L-Arg concentration in the microenvironment could represent an important mechanism to modulate the expression of CD3zeta and the T cell receptor and consequently of T cell function.

* This work was supported in part by NCI, National Institutes of Health, Grant CA82689-01, CA88885-01, and R21 CA831198.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed: Tumor Immunology Program, Stanley S. Scott Cancer Center and Dept. of Pediatrics, Louisiana State University, Health Sciences Center, 533 Bolivar St., Rm. 455, New Orleans, LA 70112. Tel.: 504-599-0914; Fax: 504-599-0864; E-mail: aochoa@lsuhsc.edu.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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