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Co-stimulation of TLR4 and Dectin-1 Induces the Production of Inflammatory Cytokines but not TGF-${\beta}$ for Th17 Cell Differentiation

  • Chang, JiHoon (Department of Microbiology and Immunology, The University of Michigan Medical School) ;
  • Kim, Byeong Mo (Division of Gerontology, Department of Medicine, Beth Israel Deaconess Medical Center) ;
  • Chang, Cheong-Hee (Department of Microbiology and Immunology, The University of Michigan Medical School)
  • Received : 2014.01.28
  • Accepted : 2014.02.05
  • Published : 2014.02.28
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Abstract

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-${\beta}$. 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-${\beta}$ but not IL-6 or IL-$1{\beta}$ 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-${\beta}$ production is a limiting factor for promoting Th17 immunity.

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References

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