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자료유형
학술저널
저자정보
저널정보
대한면역학회 Immune Network Immune Network Vol.14 No.1
발행연도
2014.2
수록면
30 - 37 (8page)

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Collaboration of TLR and non-TLR pathways in innate immune cells, which acts in concert for the induction of inflammatory cytokines, can mount a specific adaptive immune response tailored to a pathogen. Here, we show that murine DC produced increased IL-23 and IL-6 when they were treated with LPS together with curdlan that activates TLR4 and dectin-1, respectively. We also found that the induction of the inflammatory cytokine production by LPS and curdlan requires activation of IKK. However, the same treatment did not induce DC to produce a sufficient amount of TGF-β. As a result, the conditioned media from DC treated with LPS and curdlan was not able to direct CD4<sup>+</sup> T cells to Th17 cells. Addition of TGF-β but not IL-6 or IL-1β was able to promote IL-17 production from CD4<sup>+</sup> T cells. Our results showed that although signaling mediated by LPS together with curdlan is a potent stimulator of DC to secrete many pro-inflammatory cytokines, TGF-β production is a limiting factor for promoting Th17 immunity.

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