How Aureobasidium pullulans β-1,3/1,6-glucan activates macrophages, NK cells, and dendritic cells through Dectin-1 and CR3 receptor pathways.
Aureobasidium pullulans beta glucan activates innate immunity by binding Dectin-1 receptors on macrophages and dendritic cells, triggering NF-κB → cytokine production (TNF-α, IL-6, IL-12). It also binds CR3 on NK cells, priming cytotoxic activity against tumor cells. A third, Dectin-1-independent pathway upregulates interferon-stimulated genes (ISGs) — providing antiviral immune priming. This triple-pathway activation is documented across 60+ peer-reviewed studies.
Beta glucan from Aureobasidium pullulans activates innate immunity via distinct but complementary pathways depending on cell type and receptor.
β-1,3/1,6-glucan binds Dectin-1 (CLEC7A) on macrophages and dendritic cells → Syk kinase → Card9 → NF-κB activation → TNF-α, IL-6, IL-12 production + enhanced phagocytosis.
Beta glucan binds Complement Receptor 3 (CR3/CD11b) on NK cells → priming for enhanced cytotoxic activity against tumor cells and virus-infected cells via perforin/granzyme release.
A third pathway documented in macrophage studies: beta glucan upregulates interferon-stimulated genes (ISGs) — OAS1, MX1, IFIT1 — independent of Dectin-1. Relevant to antiviral immune priming.
Dendritic cells activated by beta glucan produce IL-12, driving T cell differentiation toward Th1 responses. This bridge from innate to adaptive immunity is studied in the context of anti-tumor vaccine adjuvancy.
Dectin-1 activation increases macrophage phagocytic activity — the ability to engulf and destroy pathogens and dead cells. Measured by fluorescent bead uptake assays in multiple in vitro studies.
A stable isotope tracer study (²H-labeled beta glucan) confirmed intestinal absorption and detection in peripheral blood — evidence that orally administered Aureobasidium beta glucan reaches systemic immune cells.
Selected peer-reviewed studies documenting immune activation by Aureobasidium pullulans beta glucan.
60+ indexed studies with abstracts, AI summaries, DOI links, and PMID references in the Research Archive.
Open Research Archive