Journal
CARBOHYDRATE POLYMERS
Volume 219, Issue -, Pages 121-129Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.carbpol.2019.05.023
Keywords
Galectin-3; Pectin; Inhibitor; T-cell activation; T-cell apoptosis; Anti-tumor
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Funding
- National Natural Science Foundation of China [31870796, 31770852]
- China Postdoctoral Science Foundation [2018M640276]
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Galectin-3 (Gal-3) can induce T-cell activation and apoptosis and plays a role in tumor immune tolerance. Here, we demonstrate that ginseng pectins selectively inhibit Gal-3-induced T-cell apoptosis, while not affecting T-cell activation. This finding stands in contrast to that from the use of modified citrus pectin (MCP) and potato galactan (P-galactan) that inhibit both. Whereas PKC/ERK and ROS/ERK pathways are involved in both T-cell activation and apoptosis, the Ras/PI3K/Akt pathway is unique to T-cell activation. Ginseng pectins selectively inhibit the ROS/ERK pathway. Using the Sarcomar-180 mouse model in which Gal-3 expression is increased, we found that ginseng pectins (but not MCP or P-galactan) significantly promote T-cell proliferation and IL-2 expression, and inhibit tumor growth by 45%. These in vivo data correlate well with selective effects of pectins on Gal-3-mediated T-cell apoptosis and activation. Our study suggests a novel approach for the development of polysaccharide-based agents that target Gal-3 function.
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