It is well accepted that the balance of immunity between effector and regulatory T cells determines the outcome of autoimmune and chronic inflammatory diseases. Concerning the topic of ‘Regulatory and Effector T Cells’ as published in this issue of Journal of Molecular Cell Biology, several investigators have provided important new information.
    T-helper 1 (Th1) and Th2 cells represent the classical type of Th or effector cells. However, recent studies have also identified several new cell subsets of Th cells, including IL-9-producing T (Th9), IL-17-producing T (Th17), IL-22-producing T (Th22), and T follicular helper (Tfh) cells, extending the Th cell structure. Given their crucial role in the pathogenesis of autoimmune and inflammatory diseases, Th17 cells have received much attention. They mainly express IL-17A, but co-express IL-17B, IL-17E (IL-25), IL-17F, and IL-22. IL-26 is produced by human but not mouse Th17 cells. IL-17A is significantly more potent in initiating signaling and causing autoimmune responses than other cytokines produced by these cells. The differentiation of mouse Th17 cells needs the combination of IL-6 and transforming growth factor-beta (TGF-β) (Bettelli et al., 2006), although IL-6- or TGF-β-independent pathways may also contribute to Th17 cell differentiation. The role of TGF-β in human Th17 cell differentiation is still controversial. Of note, the IL-21 and IL-1 signal pathways seem to be important in initiating Th17 cell development. IL-21 and IL-23 are also known to sustain and expand Th17 cells.
    Dr Ryffel's group provides an updated account of the differentiation and function of Th17 cells, particularly during lung injury and inflammatory disease. They demonstrated that lung injury or allergen exposure leads to NLPR3 activation, with formation of the NLPR3 inflammasome complex and caspase-1 activation resulting in mature IL-1β, which may elicit IL-17 production.