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Mechanism of tumor cell-induced T-cell apoptosis mediated by galectin-1.

par Kovács-Sólyom, Ferenc;Blaskó, Andrea;Fajka-Boja, Roberta;Katona, Róbert L;Végh, Lea;Novák, Julianna;Szebeni, Gábor János;Krenács, László;Uher, Ferenc;Tubak, Vilmos;Kiss, Robert ;Monostori, Eva
Référence Immunology letters, 127, 2, page (108-118)
Publication Publié, 2010-01

Article révisé par les pairs

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Résumé :

Galectin-1 (Gal-1) has been implicated in tumor progression partly via the induction of T-cell apoptosis. However the mechanism of Gal-1 induced T-cell death was mostly studied using recombinant, soluble Gal-1 producing controversial results. To explore the true mechanism of Gal-1 and hence tumor cell-induced T-cell death, we applied co-cultures of tumor cells and T-cells thus avoiding artificial circumstances generated using recombinant protein. T-cells died when co-cultured with Gal-1-expressing but survived with Gal-1 non-expressing tumor cells. Removing tumor cell surface Gal-1 or knocking down Gal-1 expression resulted in diminution of T-cell apoptosis. Gal-1 transgenic or soluble Gal-1 treated HeLa cells became cytotoxic. Stimulation of apoptosis required interaction between the tumor and T-cells, presence of p56lck and ZAP70, decrease of mitochondrial membrane potential and caspase activation. Hence tumor cell-derived Gal-1 might efficiently contribute to tumor self-defense. Moreover this system resolves the discrepancies obtained using recombinant Gal-1 in T-cell apoptosis studies.