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Sci. Signal., 6 December 2011
Vol. 4, Issue 202, p. ra85
[DOI: 10.1126/scisignal.2001637]

RESEARCH ARTICLES

Editor's Summary

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.

Citation: T. Tanaka, Y. Yamamoto, R. Muromoto, O. Ikeda, Y. Sekine, M. J. Grusby, T. Kaisho, T. Matsuda, PDLIM2 Inhibits T Helper 17 Cell Development and Granulomatous Inflammation Through Degradation of STAT3. Sci. Signal. 4, ra85 (2011).

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THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
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R. A. Bowe, O. T. Cox, V. Ayllon, E. Tresse, N. C. Healy, S. J. Edmunds, M. Huigsloot, and R. O'Connor (2014)
Mol. Biol. Cell 25, 184-195
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