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Immune receptors for polysaccharides from Ganoderma lucidum
Bao-Mei Shao1, Hui Dai, Wen Xu
1Department of Immunology, Peking University Health Science Center, School of Basic Medical Sciences, Beijing, China.
Biochemical and Biophysical Research Communications
|September 8, 2004
Summary
Ganoderma lucidum polysaccharides (GLPS) activate immune cells by interacting with Toll-like receptor 4 (TLR4) and membrane immunoglobulin on B cells, and TLR4 on macrophages. This reveals key mechanisms for traditional Chinese medicine immune enhancement.
Area of Science:
- Immunology
- Pharmacology
- Traditional Chinese Medicine
Background:
- Ganoderma lucidum (GL) is a medicinal fungus used in Traditional Chinese Medicine for its immune-enhancing and anti-tumor properties.
- The precise molecular mechanisms by which GL polysaccharides (GLPS) exert their immunomodulatory effects are not fully understood.
- Identifying immune receptors for GLPS is crucial for understanding its therapeutic potential.
Purpose of the Study:
- To identify and characterize the immune receptors responsible for GLPS-mediated immune cell activation.
- To elucidate the molecular pathways involved in GLPS-induced B cell and macrophage activation.
- To explore the role of Toll-like receptor 4 (TLR4) in GLPS immune responses.
Main Methods:
- In vitro activation assays using BALB/c and C3H/HeJ mouse B cells and macrophages.
- Proliferation assays and monoclonal antibody inhibition studies targeting TLR4 and immunoglobulin (Ig).
- Macrophage-polysaccharide binding inhibition assays and IL-1beta production measurements.
- Co-precipitation experiments to identify GLPS-binding proteins.
Main Results:
- GLPS activated BALB/c mouse B cells and macrophages, but not T cells.
- GLPS failed to activate B cells from C3H/HeJ mice (mutated TLR4), and TLR4 inhibition blocked GLPS-induced B cell proliferation.
- Both membrane Ig and TLR4 are necessary for GLPS-mediated B cell activation.
- GLPS inhibited macrophage binding to Astragalus membranaceus polysaccharides and induced IL-1beta production in a TLR4-dependent manner.
- GLPS binding proteins, including serum protein, ribosomal protein S7, and a transcriptional coactivator, were identified.
Conclusions:
- Toll-like receptor 4 (TLR4) and membrane immunoglobulin are critical receptors for GLPS-mediated B cell activation.
- TLR4 is also involved in GLPS-induced macrophage activation and IL-1beta production.
- These findings provide insights into the molecular mechanisms of immunopotentiation by GLPS, relevant to Traditional Chinese Medicine.