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KMID : 0923620140140010030
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Immune Network
2014 Volume.14 No. 1 p.30 ~ p.37
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Co-stimulation of TLR4 and Dectin-1 Induces the Production of Inflammatory Cytokines but not TGF-β for Th17 Cell Differentiation
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Chang Ji-Hoon
Kim Byeong-Mo
Chang Cheong-Hee
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Abstract
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Collaboration of TLR and non-TLR pathways in innate im-mune cells, which acts in concert for the induction of in-flammatory 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 treat-ed 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 re-quires 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＋ 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＋ 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 promot-ing Th17 immunity.
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KEYWORD
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TLR, Dectin-1, IL-17, TGF-β
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