期刊
IMMUNOLOGY LETTERS
卷 127, 期 2, 页码 108-118出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.imlet.2009.10.003
关键词
Galectin-1; Tumor cells; Tumor-associated stroma cells; T-cell apoptosis
类别
资金
- Hungarian Scientific Research Fund [OTKA K 69047, PD 75938, NKTH-OTKA CK 78188, CK 78007]
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 tumorcells 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. (C) 2009 Elsevier B.V. All rights reserved.
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