Zymosan Depleted - Dectin-1 Agonist

Zymosan depleted was obtained by treating zymosan with hot alkali to remove all its TLR-stimulating properties. Zymosan depleted activates Dectin-1 but not TLR2. Dectin-1, which is expressed on phagocytes, is a specific receptor for β-glucans [1]. β-Glucans are glucose polymers found in the cell walls of fungi, such as zymosan (a cell wall preparation of Saccharomyces cerevisiae) and Candida albicans. Dectin-1 binds and internalizes β-glucans and mediates the production of reactive oxygen species (ROS), activation of NF-κB and subsequent secretion of proinflammatory cytokines. However, it is now clear that its β-glucan moiety triggers NF-κB activation only through Dectin-1 as treatment with hot alkali or organic solvents abrogates the TLR2-dependent response [2,3]. RAW-Blue™ cells express high levels of endogenous Dectin-1 and therefore can be used as a Dectin-1 reporter cell line. Stimulation of RAW-Blue™ cells with zymosan depleted or heat-killed preparations of yeast induces the activation of NF-κB in a Dectin-dependent manner. NF-κB activation can be readily monitored as RAW-Blue™ cells stably express an NF- κB-inducible SEAP reporter gene. 

References:
1. Brown GD. et al., 2003. Dectin-1 mediates the biological effects of beta-glucans. J Exp Med. 197( 9): 1119- 24. 
2. Gantner BN. et al., 2003. Collaborative induction of inflam- matory responses by dectin-1 and Toll- likereceptor 2. J Exp Med. 197( 9): 1107- 17. 
3. 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.