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자료유형
학술저널
저자정보
Shin, Seul-Mee (College of Pharmacy, Sahmyook University) Jung, Ki-Sung (College of Pharmacy, Chungbuk National University) Park, Yoon-Hee (College of Pharmacy, Sahmyook University) Ko, Young-Wook (College of Pharmacy, Sahmyook University) Lee, Chong-Kil (College of Pharmacy, Chungbuk National University) Cho, Kyung-Hae (Department of Biology, Seoul Women's University) Ha, Nam-Joo (College of Pharmacy, Sahmyook University) Kim, Kyung-Jae (College of Pharmacy, Sahmyook University)
저널정보
한국응용약물학회 Biomolecules & Therapeutics(구 응용약물학회지) Biomolecules & therapeutics 제19권 제1호
발행연도
2011.1
수록면
77 - 83 (7page)

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Sulforaphane is an isothiocyanate found in cruciferous vegetables that has been reported to be an effective cancer preventive agent inducing growth arrest and/or cell death in cancer cells of various organs. This paper reports that sulforaphane exerts immunomodulatory activity on the MHC-restricted antigen presenting function. Sulforaphane efficiently increased the class II-restricted presentation of an exogenous antigen, ovalbumin (OVA), in both dendritic cells (DCs) and peritoneal macrophages in vitro. The class II-restricted OVA presentation-enhancing activity of sulforaphane was also confirmed using mice that had been injected with sulforaphane followed by soluble OVA. On the other hand, sulforaphane did not affect the class I-restricted presentation of exogenous OVA at concentrations that increase the class II-restricted antigen presentation. At a high concentration ($20\;{\mu}M$), sulforaphane inhibited the class I-restricted presentation of exogenous OVA. Sulforaphane did not affect the phagocytic activity of the DCs, and the cell surface expression of total H-$2K^b$, B7-1, B7-2 and CD54 molecules, even though it increased the expression of I-$A^b$ molecules to a barely discernable level. These results show that sulforaphane increases the class II-restricted antigen presenting function preferentially, and might provide a novel insight into the mechanisms of the anti-cancer effects of sulforaphane.

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