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Apigenin Inhibits Immunostimulatory Function of Dendritic Cells: Implication of Immunotherapeutic Adjuvant

College of Pharmacy, Pusan National University, Busan, Korea (J.S.L., H.Y.C.); and National Research Laboratory of Dendritic Cells Regulation and Medical Research Institute (Y.-I.J., C.-M.L., Y.M., Y.-M.P.) and Departments of Microbiology and Immunology (Y.-I.J., C.-M.L., Y.M., Y.-M.P.), Obstetrics and Gynecology (M.-S.Y., B.-M.C., J.-H.P.), and Thoracic Cardiovascular Surgery and Gynecology (S.-C.S., S.K.L., Y.H.C.), College of Medicine, Pusan National University, Pusan, Korea

Apigenin, one of the most common flavonoids, has been shown to possess anti-inflammatory, anticarcinogenic, and free radical-scavenging properties. However, the influence of apigenin on the immunostimulatory effects and maturation of dendritic cells (DC) remains, for the most part, unknown. In this study, we have attempted to ascertain whether apigenin influences the expression of surface molecules, dextran uptake, cytokine production, and T-cell differentiation as well as the signaling pathways underlying these phenomena in murine bone marrow-derived DC. In the presence of apigenin, CD80, CD86, and major histocompatibility complex class I and II molecules, expressions on DC were significantly suppressed, and lipopolysaccharide (LPS)-induced interleukin (IL)-12 expression was impaired. The DC proved highly efficient at antigen capture, as evidenced by the observation of mannose receptor-mediated endocytosis in the presence of apigenin. The LPS-induced activation of mitogen-activated protein kinase, the nuclear translocation of its nuclear factor-B p65 subunit, and the induction of the T-helper 1 response were all impaired in the presence of apigenin, whereas the cell-mediated immune response remained normal. These findings provide new insight into the immunopharmacological functions of apigenin and its effects on DC, and they may also prove useful in the development of adjuvant therapies for individuals suffering from acute or chronic DC-associated diseases.

Received for publication March 15, 2006.

Accepted for publication June 16, 2006.

Address correspondence to: Dr. Yeong-Min Park, Department of Microbiology and Immunology and National Research Laboratory of Dendritic Cell Regulation, Pusan National University College of Medicine, Ami-dong 1-10, Seo-gu, Pusan 602-739, South Korea. E-mail: immunpym{at}pusan.ac.kr