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Curdlan activates dendritic cells through dectin-1 and toll-like receptor 4 signaling

2016; Elsevier BV; Volume: 39; Linguagem: Inglês

10.1016/j.intimp.2016.07.013

1878-1705

Hyung Sook Kim, Ki Hwan Park, Hong Kyung Lee, Ji Sung Kim, Yong Guk Kim, Jae Hee Lee, Ki Hun Kim, Jieun Yun, Bang Yeon Hwang, Jin Tae Hong, Young Soo Kim, Sang‐Bae Han,

Immune Cell Function and Interaction

Curdlan, a β-1,3-glucan isolated from Alcaligenes faecalis, is an agonist of dectin-1 in various immune cells, including dendritic cells (DCs). However, whether curdlan also activates DCs through other receptors remains unknown. In this study, we found that curdlan activates DCs through dectin-1 and toll-like receptor 4 (TLR4). Curdlan increased the expression levels of surface molecules (CD40, CD80, CD86, and MHC-I/II), the production of cytokines (IL-12, IL-1β, TNF-α, and IFN-β), migration toward MIP-3β, and allogeneic T cell stimulation activity of DCs. Curdlan increased the phosphorylation of Syk, Raf-1, Akt, MAPKs, IKK, and NF-κB p65 in DCs. However, curdlan only slightly activated DCs transfected with small interfering RNAs against dectin-1 or TLR4 and C3H/HeJ DCs, which have non-functional TLR4, in comparison with control DCs. Curdlan increased antitumor activity of DCs in a syngeneic tumor model. In summary, our data show that curdlan activates DCs through dectin-1 and TLR4 signaling and the combination of curdlan and DCs efficiently inhibit tumor growth in mice.