Persistence, Pathogenicity and Plasticity: The Role of IL-23 in Th17 Fate

For a long time Th1 cells were considered the key players in the induction of inflammation and progression of disease in autoimmune diseases. With the discovery of IL-17-producing CD4 + T cells (Th17) being abundant at inflammation sites, this soon changed. Investigating this new T helper subset, it became clear that in comparison to Th1 and Th2 cells, Th17 cells have an increased tendency to change their phenotype and therefore become either more pathogenic or immunoregulatory. This makes them an attractive target for therapeutic interventions. As plasticity of Th17 cells differs between different autoimmune diseases, understanding its drivers is complex. This review focusses on the role of plasticity within Th17 cells in induction, aggravation and resolution of disease and points out IL-23 as a potential key player in controlling Th17 fate. Finally, current treatments targeting IL-23 and Th17 plasticity are highlighted and an outlook on future therapeutics is given.