B10 cells suppress immune responses by secreting interleukin 10 (IL-10); however, their number and function are dysregulated in rheumatoid arthritis (RA), as tumor necrosis factor-alpha (TNF-α) downregulates IL-10 and upregulates IFN-γ and IL-17A, inducing a proinflammatory B10 cell phenotype, leading to disease deterioration (76). Here, IL17A is linked to rheumatoid arthritis.