Journal
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 39, Issue -, Pages 71-78Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.intimp.2016.07.013
Keywords
Adjuvant; Cancer immunotherapy; C3H/HeJ; siRNA
Categories
Funding
- Korean government [NRF-2008-0062275, MOTIE-1415139249]
- Korean government (Functional Districts of the Science Belt Support program)
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Curdlan, a beta-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-1 beta, TNF-alpha, and IFN-beta), migration toward MIP-3 beta, and allogeneic T cell stimulation activity of DCs. Curdlan increased the phosphorylation of Syk, Raf-1, Akt, MAPKs, IKK, and NF-kappa B 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. (C) 2016 Elsevier B.V. All rights reserved.
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