Targeting the IL-17/IL-23 axis in chronic inflammatory immune-mediated diseases

The advent of a variety of cytokine inhibitors in the treatment of autoimmune and autoinflammatory diseases has transformed the clinical outlook in recent years. However, a proportion of patients either does not respond or exhibits only partial or short-lived benefits. As such, there remains intense interest in identifying new pathways that can yield therapeutic benefit when modulated. The IL-17 pathway has been identified in murine models as a potent driver of autoimmune phenomena. IL-17 family cytokines are released by a several leukocyte subsets, primarily T cells and innate lymphocytes. In turn, this family is induced by a variety of upstream cytokines, including IL-23. Several clinical trials have now identified marked benefits upon inhibition of the IL-17/IL-23 axis, particularly in psoriasis. Such data are being extended in a variety of clinical inflammatory diseases with variable benefit arising, including potential deficit. It is likely that agents that target IL-17 and IL-23 will find a place in the management of psoriasis initially with other disease states emerging over time