Abstract Title:

Fucoidin enhances dendritic cell-mediated T-cell cytotoxicity against NY-ESO-1 expressing human cancer cells.

Abstract Source:

Biochem Biophys Res Commun. 2010 Feb 12 ;392(3):329-34. Epub 2010 Jan 11. PMID: 20067767

Abstract Author(s):

Yaling Hu, Samuel Chak-Sum Cheng, Kin-Tak Chan, Yan Ke, Bofu Xue, Fion Wan-Yee Sin, Chenjie Zeng, Yong Xie

Article Affiliation:

Department of Biology, The Hong Kong University of Science and Technology, Kowloon, Hong Kong SAR, China.

Abstract:

Scavenger receptor A (SR-A) plays a crucial role in affecting the dendritic cell-mediated presentation of cancer testis antigens to T cells against human cancer cells. Here we use a dendritic cell-mediated model to verify that a sulphated polysaccharide, fucoidin, can regulate the adverse regulatory function of SR-A, and lead to the up-regulation of the anti-tumor immunological response. SR-A is a receptor of calreticulin (CRT) existing on the surface of dendritic cells (DCs). CRT is a specific receptor for a NY-ESO-1 cancer testis antigen, and CRT itself is responsible for the cross-presentation of NY-ESO-1 to CD8+ cells and the induction of anti-tumor immunity. Flow cytometrical analysis (FACS) showed that fucoidin was able to significantly enhance the binding ratio of NY-ESO-1 to human DCs in a concentration dependent manner, and that the addition of fucoidin promoted the DC maturation upon stimulation of NY-ESO-1. Results from a cytotoxicity assay indicated that fucoidin-treated DCs stimulated the CD8+ T cells more effectively than non-treated DCs via a cross-presentation pathway. Furthermore, it was found that after stimulated by fucoidin-treated DCs, the CD8+ T cells can release more IFN-gamma than non-fucoidin-treated cells as detected by intracellular IFN-gamma staining. We conclude that fucoidin enhances the cross-presentation of NY-ESO-1 to T cells leading to an increase of T-cell cytotoxicity against NY-ESO-1 expressing human cancer cells.

Study Type : In Vitro Study

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