In other immune-mediated diseases, such as rheumatoid arthritis (RA), the active metabolite calcitriol reduces the proinflammatory profile of CCR6+ memory T helper cells—producers of IL-17A, IFN-γ, and TNF-α—and induces the expression of IL-10 and CTLA4, giving them regulatory properties without affecting their migratory capacity to inflammatory environments such as synovial fluid [54]. This evidence concerns the gene IL10 and rheumatoid arthritis.