Psoriatic Arthritis

Let’s take a closer look at the pathogenesis of psoriatic arthritis. Injury, infection, or other idiopathic reasons, activate the innate immune system, in this case, dendritic cells. These activated dendritic cells function as antigen presenting cells and produce IL-12 and IL-23 cytokines. IL-12 mediates the differentiation of naïve T cells to T helper 1 cells which produce interferon-γ and TNFα. IL-23 induces differentiation of naïve T cells to T helper 17 cells, which produce IL-17, TNFα, and IL-22 and can cause inflammation, joint erosion, and new bone formation. In addition to IL-23 mediated T helper 17 cell activation, there are many other cell types that produce IL-17, several of them independent of IL-23 stimulation, including natural killer cells, mast cells, neutrophils, and innate lymphoid cells. Ixekizumab and secukinumab are two IL-17a-specific monoclonal antibodies, which prevent the cytokine from binding to its receptor, attenuating the inflammatory response.