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A more recent version of this article appeared on September 1, 2003

Published online before print June 16, 2003
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© 2003 by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0602293

Received for publication June 12, 2002.
Revised February 4, 2003.
Accepted for publication February 12, 2003.

Article

Nitric oxide-mediated inhibition of caspase-dependent T lymphocyte proliferation

Raja S. Mahidhara @, Rosemary A. Hoffman , Sulan Huang , Amanda Wolf-Johnston , Yoram Vodovotz , Richard L. Simmons , and Timothy R. Billiar

Department of Surgery, University of Pittsburgh School of Medicine, Pennsylvania

@ To whom correspondence should be addressed. E-mail: mahidharar{at}msx.upmc.edu.


  Abstract

Nitric oxide (NO), a pleiotropic signaling molecule produced at sites of inflammation, is a powerful inhibitor of lymphocyte proliferation. Caspases, central effector proteases in apoptosis, have recently been implicated as critical mediators of T cell activation. We and others have shown that NO can inhibit caspases by S-nitrosylation, which is reversible by the reducing agent dithiothreitol (DTT). The purpose of the present study was to determine whether NO inhibits lymphocyte proliferation by modulating caspase activity. Caspase inhibition with z-VAD-fmk blocked T cell proliferation. NO-dependent inhibition of T cell proliferation was associated with an inhibition of caspase activity and activation, and this effect was reversible by DTT. Previous studies demonstrated inhibition of apoptosis through S-nitrosylation of caspases; the present studies extend this effect to inhibition of caspase-dependent T cell proliferation.

Key Words: T cell • cellular proliferation • apoptosis • S-nitrosylation




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