6533b821fe1ef96bd127c009

RESEARCH PRODUCT

Modulation of dendritic cells and macrophages : implication in cancer and atherosclerosis

subject

description

During my thesis, I studied the cytotoxic function of dendritic cells (DC) from cancer patients and compared it to DC from healthy donors. Our results indicate that human monocyte-derived DC can acquire strong cytotoxic activity toward tumor cells after activation with low dose of LPS. The cytotoxic potential of DC derived from cancer patients was almost the same as the one generated from healthy donors. We identified the tumor cell killing mechanism which involves peroxynitrite release. After killing of cancer cells, DC are capable of engulfing dead tumor cell fragments and overexpress the costimulatory molecules necessary for T cell proliferation. A second study consisted in an analysis of inflammatory macrophages and their significance in atherosclerosis. Macrophages produce CETP (cholesteryl ester transfert protein), a target for LXR (liver X receptor) receptors. Our results show that LXR-mediated induction of CETP expression is lost in inflammatory macrophages. Our study suggests that inflammatory macrophages may not increase the circulating CETP pool on LXR agonist treatment.