The influence of berberine on co-stimulatory molecule expression and T cell activation

Abstract Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation and deterioration within the joints, as well as extra-articular and systemic manifestations depending on severity. While there are many immunological factors that contribute to the pathology of RA, its progression is largely due to the activation of CD4+ T cells by antigen presenting cells (APCs), which then subsequently enhances the immune response of other cells within the area. Berberine (BBR), an isoquinoline alkaloid, has demonstrated the ability to attenuate mechanisms involved in RA in vitro and in vivo. Recent studies provide some evidence that BBR may interfere with the co-stimulatory mechanisms involved in a RA inflammatory response, however research specifically concerning BBR’s effect on co-stimulatory molecule expression and IL-12 production remains equivocal. In this study, we used flow cytometry to examine BBR’s effect on the cell surface expression of co-stimulatory molecules on bone marrow-derived dendritic cells (BMDCs) following stimulation with LPS, and on isolated splenic CD4+ T cells following activation with anti-CD3/anti-CD28. On BMDCs, the expression of CD40, CD80/86, and MHC class II was quantified, whereas CD40L, CD28, and IL-2R expression was examined on splenic CD4+ T cells. The amount of IL-12 secreted in BMDC supernatant was measured with an ELISA. The data collected on BBR’s effects will allow further insight into its potential as an alternative therapy for RA.