Mechanism of CD83 expression induction through dectin-1 and β-glucan interaction in innate immune responses.

This study assessed how the interaction between human monocyte dectin-1 and β-glucan induces CD83 expression using THP-1 cells as a model. Flow cytometry and enzyme-linked immunosorbent assay (ELISA) were used to assess the dynamics of membrane-bound CD83 (mCD83) and soluble CD83 (sCD83) expression. Insoluble β-glucan induced CD83 expression more effectively than that of soluble β-glucan. Additionally, our findings indicate that the activation of nuclear factor-kappa B (NFκB) and nuclear factor of activated T cells (NFAT) plays a crucial role in the dectin-1 signaling pathway. sCD83 production is driven by metalloproteinases following mCD83 expression and inhibits mCD83 expression. This study offers novel insights into the immunoregulatory role of CD83 and its regulatory mechanisms, highlighting potential strategies for treating fungal infections and autoimmune diseases.