Beta-glucosylceramide (β-GlcCer) is a naturally occurring glycolipid that specifically activates the macrophage-inducible C-type lectin (Mincle) receptor [1]. Mincle is a member of the Dectin-2 family, that recognizes a variety of exogenous and endogenous stimuli, such as mycobacteria, certain fungi, and necrotic cells.
β-GlcCer is an intracellular metabolite which is recognized as a damage-associated molecular pattern (DAMP) and associated with cell death [1, 2].
In healthy individuals, β-GlcCer is located in the endoplasmic reticulum/Golgi apparatus. Following cell damage, it is released into the extracellular milieu where it acts as a signal of cell damage. Of note, the accumulation of β-GlcCer within cells is believed to cause systemic inflammation in Gaucher disease [1].
Using InvivoGen's HEK‑Blue™ Mincle reporter cells, β-GlcCer was established as an endogenous Mincle agonist [1]. Upon β-GlcCer recognition, Mincle interacts with the Fc receptor common γ-chain (FcRγ) triggering Syk‑dependent signaling resulting in NF-κB, NFAT, and AP-1 activation. Of note, NF-κB activation by synthetic β-GlcCer was found to be comparable to that induced by the mycobacteria-derived TDM, an extensively studied exogenous Mincle agonist [1].
Due to its pro-inflammatory activity, β-GlcCer has been identified as a potential adjuvant for vaccination against infectious diseases and cancer [1].
Key highlights of β-GlcCer:
- Endogenous and specific Mincle agonist
- Activates NF-κB, NFAT, and AP-1
- Each lot of β-GlcCer is highly pure (≥95%) and functionally tested
InvivoGen's β-GlcCer is a synthetic glycosylceramide bearing an unsaturated long-chain (C24:1). It is of the highest quality, guaranteed free of bacterial contamination, and has been functionally validated using cellular assays.
References:
- Nagata M. et al. 2017. Intracellular metabolite β-glucosylceramide is an endogenous Mincle ligand possessing immunostimulatory activity. PNAS. 114(16): E3285-E3294.
- Ishikawa A. et al. 2019. Essential roles of C-type lectin Mincle in induction of neuropathic pain in mice. Sci Rep. 9(1):872.
