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[Mannan-Binding Lectin Inhibits Candida Albicans-Induced DC Maturation and Cytokine Secretion]
Ming-Yong Wang1,2, Fan-Ping Wang2, Jing-Jing Zhai2
1Sanquan Medical College, Xinxiang Medical University, Xinxiang 453003, Henan Province, China.
Zhongguo Shi Yan Xue Ye Xue Za Zhi
|May 8, 2015
Summary
Mannan-binding lectin (MBL) inhibits Candida albicans-induced immune responses in dendritic cells by reducing cytokine production and NF-κB signaling. This suggests MBL regulates the immune response to C. albicans.
Area of Science:
- Immunology
- Cell Biology
Background:
- Dendritic cells (DCs) are crucial in initiating immune responses.
- Candida albicans (C. albicans) is a fungal pathogen that can trigger immune responses via DCs.
- Mannan-binding lectin (MBL) is a key component of the innate immune system involved in pathogen recognition.
Purpose of the Study:
- To investigate the impact of MBL on the maturation and cytokine secretion of human dendritic cells (DCs) stimulated by C. albicans.
- To elucidate the molecular mechanisms underlying MBL's effects on DCs during C. albicans infection.
Main Methods:
- Human peripheral blood mononuclear cells were differentiated into monocyte-derived dendritic cells (MoDCs).
- MoDCs were stimulated with C. albicans in the presence of varying MBL concentrations.
- DC maturation markers (CD83, CD86), cytokine levels (TNF-α, IL-6), MBL-DC/C. albicans interaction, IκBα phosphorylation, and p65/NF-κB translocation were analyzed using FACS, ELISA, and Western blot.
Main Results:
- MBL, particularly at higher concentrations (10-20 mg/L), down-regulated CD83 and CD86 expression on C. albicans-stimulated MoDCs.
- MBL inhibited the production of TNF-α and IL-6 induced by C. albicans.
- MBL demonstrated binding to both C. albicans and immature DCs in a Ca2+-dependent manner, and it reduced IκBα phosphorylation and p65/NF-κB nuclear translocation.
Conclusions:
- MBL inhibits C. albicans-induced TNF-α and IL-6 production in DCs, likely via the NF-κB signaling pathway.
- MBL plays a regulatory role in the immune response to C. albicans infections.

