Co-stimulation of TLR4 and Dectin-1 Induces the Production of Inflammatory Cytokines but not TGF-beta for Th17 Cell Differentiation.
- Author:
Jihoon CHANG
1
;
Byeong Mo KIM
;
Cheong Hee CHANG
Author Information
- Publication Type:Original Article
- Keywords: TLR; Dectin-1; IL-17; TGF-beta
- MeSH: Adaptive Immunity; Cooperative Behavior; Culture Media, Conditioned; Cytokines*; Interleukin-17; Interleukin-23; Interleukin-6; T-Lymphocytes; Th17 Cells*; Transforming Growth Factor beta*
- From:Immune Network 2014;14(1):30-37
- CountryRepublic of Korea
- Language:English
- 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-1beta 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.
