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Defects in antitumor immune responses have been associated with increased release of prostaglandin E(2) (PGE(2)) as a result of overexpression of cyclooxygenase (COX)-2 by tumors. In this report, we examine the effects of PGE(2) on antitumor CD8(+) T-cell responses generated both by cross-presenting dendritic cells and by direct priming by tumor cells. Our data show that PGE(2) inhibits dendritic cell maturation, resulting in the abortive activation of naive CD8(+) T cells, and is dependent on interleukin-10 production by dendritic cells. Interaction of tumor cells with naïve CD8(+) T cells in the presence of PGE(2) in vitro results in the induction of CD8(+) CD28(-) T cells, which fail to proliferate or exhibit effector function. In vivo, overexpression of COX-2 by tumor cells results in a decrease in number of tumor-infiltrating dendritic cells and confers the ability of tumor cells to metastasize to the tumor draining lymph nodes.

cancer research

Prevention of Both Direct and Cross-Priming of Antitumor CD8+ T-Cell Responses following Overproduction of Prostaglandin E2 by Tumor Cells<i>In vivo</i>

Prevention of Both Direct and Cross-Priming of Antitumor CD8+ T-Cell Responses following Overproduction of Prostaglandin E2 by Tumor CellsIn vivo