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RESEARCH COMMUNICATION |
a Laboratory of Cell Biology, Department of Genetics, Biology and Medical Chemistry
b Postgraduate School of Clinical Pathology, University of Torino Medical School, 10126 Torino, Italy
c Instituto de Parasitología y Biomedicina, Consejo Superior de Investigaciones Científicas, 18001 Granada, Spain
d Division of Immunology, Beth Israel Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
e Institute of Biology and Genetics, University of Ancona Medical School, 60131 Ancona, Italy
One of the functions of surface CD38 is the induction of phosphorylation of discrete cytoplasmic substrates and mobilization of cytoplasmic calcium (Ca2+). The present work addresses the issue of whether the signaling mediated via CD38 operates through an independent pathway or, alternatively, is linked to the TCR/CD3 signaling machinery. We studied the signals elicited through CD38 by the specific agonistic IB4 monoclonal antibody (mAb) by monitoring the levels of cytoplasmic Ca2+ and the induced phenotypic and functional variations in T cell growth. IB4 mAb presented the unique ability to increase cytoplasmic Ca2+ levels, which correlated with the phosphorylation of the PLC-
1. These effects were blocked by phorbol 12-myristate 13-acetate (PMA) and were dependent on the presence of a functional TCR/CD3 surface complex, no effects being recorded on mutant Jurkat cells lacking part of the CD3 structures. CD38 signaling appeared to share with TCR/CD3 the ability to induce apoptotic cell death in Jurkat T cells, an event paralleled by specific up-regulation of the Fas molecule and inhibited by cyclosporin A. CD28, a costimulatory molecule, is synergized by increasing CD38-induced apoptotic cell death. The results indicate the existence of a strong functional interdependence between CD38 and TCR/CD3.—Morra, M., Zubiaur, M., Terhorst, C., Sancho, J., Malavasi, F. CD38 is functionally dependent on the TCR/CD3 complex in human T cells. FASEB J. 12, 581–592 (1998)
Key Words: T lymphocytes • cell surface molecules • second messengers • signal transduction • apoptosis
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