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First published on June 16, 2006; DOI: 10.1124/mol.106.024547

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Received for publication March 16, 2006.
Revised June 15, 2006.
Accepted for publication June 16, 2006.

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

Man-Soo Yoon 1, Jun Sik Lee 2, Byoung moon Choi 3, Young-Il Jeong 4, Chang-Min Lee 3, Jong-Hoon Park 1, Yuseok Moon 3, Si-Chan Sung 5, Sang Kwon Lee 5, Yun Hee Chang 5, Hae Young Chung 2, Yeong-Min Park 3*

1 Department of Obstetrics and Gynecology,Pusan National University, College of Medicine 2 College of Pharmacy, Pusan National University 3 Department of Microbiology and Immunology, Pusan National University, College of Medicine 4 Department of Microbiology, Pusan National University 5 Department of Thoracic Cardiovascular Surgery and Gynecology Pusan National University, College of M

* Address correspondence to: E-mail: immunpym{at}pusan.ac.kr

Abstract

Apigenin, one of the most common flavonoids, has demonstrated antiinflammatory, anticarcinogenic, and free-radical scavenging activity. However, its influence on the immunostimulatory effects and maturation of dendritic cells (DC) remains, for the most part, unknown. In this study, we attempted to determine whether apigenin can influence 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, the expression of CD80, CD86, and MHC class I and II molecules on DC was significantly and LPS-induced IL-12 expression was impaired. The DC proved to be highly efficient in antigen capture by means of mannose receptor-mediated endocytosis in the presence of apigenin. LPS-induced activation of MAPK, the nuclear translocation of its NF-{kappa}B p65 subunit, and induction of the Th1 response were impaired in the presence of apigenin, while the cell-mediated immune response remained normal. These findings provide new insight into the immunopharmacological functions of apigenin and its effects on DC and may prove useful in the development of adjuvant therapies for individuals with acute or chronic DC-associated diseases.


Key words: Interferons, Interleukins, MAP Kinase, Jun Kinase, P38 MAP Kinase, NFkappaB




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