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*Breast Cancer
The Journal of Immunology, 1999, 162: 2631-2638.
Copyright © 1999 by The American Association of Immunologists

Potent Inhibition of CD4/TCR-Mediated T Cell Apoptosis by a CD4-Binding Glycoprotein Secreted from Breast Tumor and Seminal Vesicle Cells1

Muriel Gaubin2,*, Monica Autiero3,*, Stéphane Basmaciogullari*, Didier Métivier*, Zohar Misëhal{dagger}, Raphal Culerrier*, Anne Oudin*, John Guardiola{ddagger} and Dominique Piatier-Tonneau3,*

* Génétique Moléculaire et de Biologie du Développement, Unité Propre de Recherche 420, Centre National de la Recherche Scientifique, Villejuif, France; {dagger} Institut Fédératif de Recherche 1221, Centre National de la Recherche Scientifique, Villejuif, France; and {ddagger} International Institute of Genetics and Biophysics, Consiglio Nazionale della Ricerche, Naples, Italy

We previously isolated a CD4 ligand glycoprotein, gp17, from human seminal plasma; this glycoprotein is identical with gross cystic disease fluid protein-15 (GCDFP-15), a factor specifically secreted from primary and secondary breast tumors. The function of gp17/GCDFP-15 in physiological as well as in pathological conditions has remained elusive thus far. As a follow up to our previous findings that gp17 binds to CD4 with high affinity and interferes with both HIV-1 gp120 binding to CD4 and syncytium formation, we investigated whether gp17 could affect the T lymphocyte apoptosis induced by a separate ligation of CD4 and TCR. We show here that gp17/GCDFP-15 is in fact a strong and specific inhibitor of the T lymphocyte programmed cell death induced by CD4 cross-linking and subsequent TCR activation. The antiapoptotic effect observed in the presence of gp17 correlates with a moderate up-regulation of Bcl-2 expression in treated cells. The presence of gp17 also prevents the down-modulation of Bcl-2 expression in Bcl-2bright CD4+ T cells that is caused by the triggering of apoptosis. Our results suggest that gp17 may represent a new immunomodulatory CD4 binding factor playing a role in host defense against infections and tumors.




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