Depleted Zymosan - Dectin-1 Agonist

Hot alkali-treated zymosan

Depleted zymosan is a purified β-glucan–enriched preparation generated by subjecting zymosan, an insoluble Saccharomyces cerevisiae cell-wall extract, to hot alkali treatment. This process selectively removes TLR2-stimulating components, including mannoproteins, phospholipannans, and other alkali-labile cell-wall constituents, while preserving the underlying β-(1→3)/(1→6)-glucan scaffold. As a result, depleted zymosan retains its ability to robustly engage the C-type lectin receptor Dectin-1, leading to Syk–CARD9–dependent signaling, but exhibits minimal to no activation of TLR2 [1,2]. This makes depleted zymosan a valuable tool for dissecting Dectin-1–specific immune responses, studying β-glucan recognition, and distinguishing CLR-mediated signaling from concomitant TLR-driven pathways typically triggered by native zymosan.

Depleted zymosan offers several advantages as a Dectin-1 agonist: as a particulate β-glucan, it is efficiently phagocytosed, closely mimics the architecture of real fungal particles, and promotes the receptor clustering and phagocytic signaling events that soluble ligands are unable to induce. Recent studies support these properties: Cheng et al. (2024) showed that depleted zymosan elicits Dectin-1–dominated signaling and innate immune training profiles comparable to purified β-glucans [3], while Anaya et al. (2023) demonstrated that particulate β-glucan structure is essential for effective Dectin-1 multimerization and downstream activation [4].

Key features

• Selective Dectin-1 agonist
• Particulate β-glucan–rich preparation
• Each lot is functionally tested using Dectin-1 reporter cells

Applications

• Studying Dectin-1–specific signaling pathways
• Investigating β-glucan–dependent phagocytosis and receptor clustering
• Innate immune training and functional reprogramming
• Comparative studies of β-glucan ligands
• CLR–TLR crosstalk analysis

References:

1. Gantner BN. et al., 2003. Collaborative induction of inflammatory responses by dectin-1 and Toll- like receptor 2. J Exp Med. 197(9):1107-17.
2. Ikeda Y. et al., 2008. Dissociation of Toll-like receptor 2-mediated innate immune response to Zymosan by organic solvent-treatment without loss of Dectin-1 reactivity. Biol Pharm Bull.31(1):13-8.
3. Cheng QJ. et al., 2024. Dectin-1 ligands produce distinct training phenotypes in human monocytes through differential activation of signaling networks. Sci Rep 14(1):1454
4. Anaya EU. et al., 2023. Dectin-1 multimerization and signaling depends on fungal β-glucan structure and exposure. Biophys J. 122(18):3749-3767.