Selective effects of ginseng pectins on galectin-3-mediated T cell activation and apoptosis

Area of Science:

• Immunology
• Oncology
• Biochemistry

Background:

• Galectin-3 (Gal-3) is implicated in tumor immune tolerance by modulating T-cell activation and apoptosis.
• Existing agents like modified citrus pectin (MCP) and potato galactan (P-galactan) inhibit both T-cell activation and apoptosis.
• Understanding the distinct molecular pathways governing T-cell activation and apoptosis is crucial for developing targeted immunotherapies.

Purpose of the Study:

• To investigate the selective effects of ginseng pectins on Galectin-3 (Gal-3) mediated T-cell apoptosis and activation.
• To elucidate the specific signaling pathways targeted by ginseng pectins in T-cells.
• To evaluate the in vivo efficacy of ginseng pectins in a tumor model by assessing T-cell responses and tumor growth inhibition.

Main Methods:

• In vitro assays to assess T-cell apoptosis and activation in response to Gal-3 and different pectins.
• Analysis of key signaling pathways including PKC/ERK, ROS/ERK, and Ras/PI3K/Akt.
• In vivo studies using the Sarcomar-180 mouse model to evaluate tumor growth, T-cell proliferation, and IL-2 expression.

Main Results:

• Ginseng pectins selectively inhibited Gal-3-induced T-cell apoptosis without affecting T-cell activation, unlike MCP and P-galactan.
• Ginseng pectins were found to selectively inhibit the ROS/ERK pathway.
• In vivo, ginseng pectins significantly promoted T-cell proliferation and IL-2 expression, leading to a 45% inhibition of tumor growth.

Conclusions:

• Ginseng pectins offer a novel, selective approach to modulating Galectin-3 (Gal-3) function in T-cells.
• The selective inhibition of Gal-3-induced T-cell apoptosis by ginseng pectins presents a promising strategy for cancer immunotherapy.
• Polysaccharide-based agents targeting Gal-3 function, like ginseng pectins, represent a new avenue for developing cancer therapeutics.