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Updated: Jun 12, 2026

Development and Functional Characterization of Murine Tolerogenic Dendritic Cells
Published on: May 18, 2018
Immunosuppressive effect of quercetin on dendritic cell activation and function
Ren-Yeong Huang1, Yen-Ling Yu, Wan-Chien Cheng
1Graduate Institute of Medical Sciences and Department of Periodontology, School of Dentistry, National Defense Medical Center and Tri-Service General Hospital, Taipei, Taiwan.
Quercetin, a natural flavonoid, suppresses dendritic cell (DC) activation and function. This natural compound shows potential for treating immune disorders by inhibiting harmful immune responses.
Area of Science:
- Immunology
- Natural Products Chemistry
Background:
- Dendritic cells (DCs) are key regulators bridging innate and adaptive immunity.
- DCs are critical targets for managing detrimental immune responses.
Purpose of the Study:
- To investigate the impact of quercetin on mouse dendritic cell (DC) activation and function.
- To explore quercetin's potential as an immunosuppressive agent.
Main Methods:
- Assessed LPS-induced DC activation markers, cytokine production, and molecule expression.
- Evaluated quercetin's effects on DC endocytosis, migration, and T cell activation.
- Investigated quercetin's impact on intracellular signaling pathways (ERK, JNK, Akt, NF-kappaB).
Main Results:
- Quercetin inhibited LPS-induced DC activation, reducing pro-inflammatory cytokines and MHC class II/costimulatory molecule expression.
- Quercetin blocked DC endocytosis and LPS-induced DC migration.
- Quercetin abrogated LPS-stimulated DC-induced T cell activation in vitro and in vivo.
- Quercetin treatment prevented 2,4-dinitro-1-fluorobenzene-induced contact hypersensitivity.
- Quercetin suppressed LPS-induced activation of ERK, JNK, Akt, and NF-kappaB pathways.
Conclusions:
- Quercetin demonstrates potent immunosuppressive properties by inhibiting DC activation and function.
- Quercetin may serve as a therapeutic agent for chronic inflammation, autoimmune diseases, and transplantation.
- Quercetin's mechanism involves blocking key signaling pathways in DCs.
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