Please use this identifier to cite or link to this item:

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

Authors Hu, Yaling
Issue Date 2008
Summary Scavenger receptor A (SR-A) has been found able to negatively regulate antitumor immunity, and Fucoidin is a promising inhibitor of SR-A. Calreticulin (CRT) on dendritic cells (DC) surface is a receptor for a cancer-testis antigen (CTA), NY-ESO-1, and CRT is responsible for the cross-presentation of NY-ESO-1 to T cells and the induction of antitumor immunity, and it may interact with SR-A for the uptake of exogenous peptides. Here we tried to verify whether the inhibition of SR-A with fucoidin, could induce an up-regulation of the antitumor immunity. In my study, flow cytometrical (FACS) analysis of NY-ESO-1 binding assay showed that the application of fucoidin significantly increases the binding ratio of NY-ESO-1 to human DCs in a concentration dependent manner. FACS analysis of DC maturation markers demonstrated that fucoidin promoted DCs maturation on stimulation of NY-ESO-1. Furthermore, the cytotoxicity assay of CD8+ T cells indicated that fucoidin-treated DCs stimulate CTL more effectively than non-treated DCs through a cross-presentation pathway. Meanwhile, through intracellular IFN-γ staining, it is found that CD8+ T cells stimulated by fucoidin treated DCs release more IFN-γ than non-fucoidin treated cells. It can be concluded that fucoidin enhances the cross-presentation of NY-ESO-1 to T-cells leading to an increase of the T cell cytotoxicity against NY-ESO-1 expressing human cancer cells, and fucoidin can significantly up-regulate the antitumor immunity.
Note Thesis (M.Phil.)--Hong Kong University of Science and Technology, 2008
Language English
Format Thesis
Access View full-text via DOI
Files in this item:
File Description Size Format
th_redirect.html 337 B HTML
Copyrighted to the author. Reproduction is prohibited without the author’s prior written consent.