Abstract
In the last decade the concept of T helper (Th) 1- versus Th2-regulated immune responses has been challenged by a number of new subpopulations, including Th17 cells. These proinflammatory cells regulate protection against a variety of bacteria and fungi but have also been connected to almost all major autoimmune diseases.1 Many of the inflammatory effects of Th17 cells are mediated via proinflammatory cytokines such as their namesake, interleukin-17A (IL-17A). Although IL-17A is involved in neutrophil recruitment and host defence, it can also lead to excessive inflammation and tissue damage. The transcriptional regulation of IL-17A and other Th17 cytokines as well as their effector function have been studied extensively; post-transcriptional modifications, on the other hand, are less well understood. In a recent issue of Nature, Rutz et al.2 address exactly this aspect. They uncover a new player in Th17 function: the deubiquitinating enzyme A (DUBA), which post-transcriptionally regulates IL-17A.
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