You are currently viewing the editor's summary.
View Full TextLog in to view the full text
AAAS login provides access to Science for AAAS members, and access to other journals in the Science family to users who have purchased individual subscriptions.
Register for free to read this article
As a service to the community, this article is available for free. Existing users log in.
More options
Download and print this article for your personal scholarly, research, and educational use.
Buy a single issue of Science for just $15 USD.
LIMiting Inflammation by T Cells
Although much is known about the development of T helper 17 (TH17) cells, a proinflammatory T cell type that is important for the immune response to pathogens, comparatively little is known about how these cells are inhibited to prevent chronic inflammation and autoimmune diseases. Tanaka et al. have identified the E3 ubiquitin ligase PDLIM2 as an endogenous inhibitor of TH17 development by targeting the essential transcription factor STAT3 (signal transducer and activator of transcription 3) for destruction. Mice lacking PDLIM2 had worse inflammatory disease than did control mice, suggesting that PDLIM2 might be a therapeutic target to prevent TH17 cell–mediated inflammatory diseases.
