Lycopene suppresses the lipopolysaccharide-induced phenotypic and functional maturation of murine dendritic cells through inhibition of mitogen-activated protein kinases and nuclear factor-κB

Dendritic cells (DC) are the most potent of antigen-presenting cells. The most important function of DC is to initiate the immune response by presenting antigens to naive T lymphocytes. Currently, little is known about the basic action of lycopene in murine bone marrow (BM)-derived DC. In the present study, we have revealed that lycopene significantly attenuates the phenotypic and functional maturation of murine BM-DC, especially in lipopolysaccharide-induced DC maturation. We found that lycopene down-regulates the expression of costimulatory molecules (CD80 and CD86) and major histocompatibility complex type II molecules. We also determined that lycopene-treated DC were poor stimulators of naive allogeneic T-cell proliferation and induced lower levels of interleukin-2 in responding T cells. They also exhibited impaired interleukin-12 production. Additionally, lycopene was able to inhibit mitogen-activated protein kinases, such as ERK1/2, p38 and JNK, and the transcription factor, nuclear factor-kappaB. Assessment of the in vivo effects of lycopene may reveal an inability to induce a normal cell-mediated immune response, despite the ability of the cells to migrate to the spleen. This data provides new insight into the immunopharmacology of lycopene and suggests a novel approach to the manipulation of DC for therapeutic application.