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International Journal of Medicinal Mushrooms
Impact-faktor: 1.423 5-jähriger Impact-Faktor: 1.525 SJR: 0.433 SNIP: 0.661 CiteScore™: 1.38

ISSN Druckformat: 1521-9437
ISSN Online: 1940-4344

Volumes:
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International Journal of Medicinal Mushrooms

DOI: 10.1615/IntJMedMushr.v16.i1.10
pages 1-16

Innate Immunity Induced by Fungal β-Glucans via Dectin-1 Signaling Pathway

Dong Hee Lee
Department of Life Sciences, University of Seoul, Seoul, Korea
Ha Won Kim
Department of Life Sciences, University of Seoul Dongdaemun-gu, Jennong-dong 90, Seoul 130-743, South Korea

ABSTRAKT

Mushrooms are a highly valuable source of substances that possess unique biological properties and medicinal efficacy. Medicinal mushrooms traditionally have been used to treat cancer, fungal infections, hypertension, diabetes, inflammation, and renal disorders. Medicinal mushrooms produce high-molecular-weight β-glucans, which have antitumor and antifungal activities that stimulate innate immunity. Innate immune cells express pattern recognition receptors (PRRs) such as dectin-1, Toll-like receptors, and mannose receptors on their cell surfaces. These PRRs recognize pathogens by binding to highly conserved pathogen-associated molecular patterns such as β-glucan, mannan, and lipopolysaccharide. The immunomodulating activities of innate immune cells are augmented by the binding of β-glucans to dectin-1 that is expressed by macrophages or dendritic cells. Upon binding β-glucan, innate immune cells activate adaptive immune cells such as B and T lymphocytes or natural killer cells by secreting various cytokines such as interleukins (IL-4, IL-6) and tumor necrosis factor-α. Water-insoluble β-glucans have stronger immunostimulating activities than their water-soluble counterparts. β-glucans have antifungal activity that is similar to their anticancer activities and is mediated by binding to dectin-1, albeit by an unknown mechanism. In this review we discuss recent progress in understanding the mechanisms responsible for the antitumor activities of fungal β-glucans that act through pathogen-associated molecular patterns and PRRs.


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