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      KCI등재 SCOPUS SCIE

      Ellagic Acid Modulates LPS-Induced Maturation of Dendritic Cells Through the Regulation of JNK Activity

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      https://www.riss.kr/link?id=A107538098

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      Ellagic acid (EA) is a well-known phytochemical that modulates various cellular processes. It is present in a variety of foods, including grapes, strawberries, and nuts. However, the influence of EA on immunological responses is not well defined. Here, we investigated the effects of EA on the lipopolysaccharide (LPS)-induced bone marrow-derived dendritic cells (BMDCs). EA was not cytotoxic to DCs. EA suppressed LPS-induced expression of costimulatory molecules (CD80 and CD86), but it did not suppress the expression of major histocompatibility complex (MHC) class I and MHC class II in BMDCs. In particular, EA blocked LPS-induced c-Jun N-terminal kinase (JNK) activation. LPS-mediated expression of proinflammatory cytokines (IL-12 and IFN-${\gamma}$) was diminished by EA. We also confirmed that levels of IL-12 and IFN-${\gamma}$ were not influenced by EA in the presence of a JNK inhibitor. Taken together, these data demonstrate that EA regulates the immune response through the modulation of LPS-induced DC maturation.
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      Ellagic acid (EA) is a well-known phytochemical that modulates various cellular processes. It is present in a variety of foods, including grapes, strawberries, and nuts. However, the influence of EA on immunological responses is not well defined. Here...

      Ellagic acid (EA) is a well-known phytochemical that modulates various cellular processes. It is present in a variety of foods, including grapes, strawberries, and nuts. However, the influence of EA on immunological responses is not well defined. Here, we investigated the effects of EA on the lipopolysaccharide (LPS)-induced bone marrow-derived dendritic cells (BMDCs). EA was not cytotoxic to DCs. EA suppressed LPS-induced expression of costimulatory molecules (CD80 and CD86), but it did not suppress the expression of major histocompatibility complex (MHC) class I and MHC class II in BMDCs. In particular, EA blocked LPS-induced c-Jun N-terminal kinase (JNK) activation. LPS-mediated expression of proinflammatory cytokines (IL-12 and IFN-${\gamma}$) was diminished by EA. We also confirmed that levels of IL-12 and IFN-${\gamma}$ were not influenced by EA in the presence of a JNK inhibitor. Taken together, these data demonstrate that EA regulates the immune response through the modulation of LPS-induced DC maturation.

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