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Sci. Signal., 27 November 2012
Vol. 5, Issue 252, p. ra87
[DOI: 10.1126/scisignal.2003365]

RESEARCH ARTICLES

Editor's Summary

Tipping Both Sides of the Inflammatory Scales
Autoimmune disorders arise because of an imbalance in the immune response. For example, effector T cells can exhibit enhanced activation, causing damaging, proinflammatory responses, whereas regulatory T cells (Tregs), which inhibit effector T cell responses, may become less effective at immunosuppression. Brownlie et al. investigated a role in the immune response for PTPN22, a protein tyrosine phosphatase implicated in autoimmunity in humans and mice. Although PTPN22-deficient mice had more potent effector T cells, they did not develop autoimmunity because they also had Tregs with greater immunosuppressive function than those of wild-type mice. Together, these data suggest that manipulating PTPN22 function in human Tregs may help in the treatment of autoimmune diseases.

Citation: R. J. Brownlie, L. A. Miosge, D. Vassilakos, L. M. Svensson, A. Cope, R. Zamoyska, Lack of the Phosphatase PTPN22 Increases Adhesion of Murine Regulatory T Cells to Improve Their Immunosuppressive Function. Sci. Signal. 5, ra87 (2012).

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THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Science Signaling Podcast: 27 November 2012.
R. Zamoyska and A. M. VanHook (2012)
Science Signaling 5, pc27
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