One of the main focuses of RA adaptive immunity has been the role of helper T-cell type 17 (TH17) which releases the pro-inflammatory cytokine IL-17.56 IL-17 is present in high levels in RA synovial fluid57 and its crucial role in the pathogenesis of RA has been demonstrated in studies where IL-17 deficient mice do not develop RA.58 Notably in 2017, Pfeifle et al.59 showed that IL-23 activated TH17 cells can also release IL-21 and 22 which interferes with B-cell antibody IgG sialylation and results in subsequent production of a type of pathogenic ACPA. Here, IL21 is linked to rheumatoid arthritis.