RT Journal Article
SR Electronic
T1 Apigenin Inhibits Immunostimulatory Function of Dendritic Cells: Implication of Immunotherapeutic Adjuvant
JF Molecular Pharmacology
JO Mol Pharmacol
FD American Society for Pharmacology and Experimental Therapeutics
SP 1033
OP 1044
DO 10.1124/mol.106.024547
VO 70
IS 3
A1 Yoon, Man-Soo
A1 Lee, Jun Sik
A1 Choi, Byoung-Moon
A1 Jeong, Young-Il
A1 Lee, Chang-Min
A1 Park, Jong-Hoon
A1 Moon, Yuseok
A1 Sung, Si-Chan
A1 Lee, Sang Kwon
A1 Chang, Yun Hee
A1 Chung, Hae Young
A1 Park, Yeong-Min
YR 2006
UL http://molpharm.aspetjournals.org/content/70/3/1033.abstract
AB 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-κB 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. The American Society for Pharmacology and Experimental Therapeutics