Similarly, RA generates a significant increase in IL-17, which is associated with CD4+ T cells that promote inflammation, bone erosion, and cartilage degradation by the stimulating expression of NF-κB-specific activator receptor ligand (RANKL) and produce IL-17, which stimulates synovial macrophages and FLS [26,27] and to plasma cells that also promote inflammation through the production of cytokines and autoantibodies [14,28]; treatments based on extracts and fractions of B. ternifolia decreased the level of IL-17, particularly M3. This evidence concerns the gene IL17A and rheumatoid arthritis.