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


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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The autoimmune-associated genetic variant PTPN22 R620W enhances neutrophil activation and function in patients with rheumatoid arthritis and healthy individuals.
R. Bayley, K. A. Kite, H. M. McGettrick, J. P. Smith, G. D. Kitas, C. D. Buckley, and S. P. Young (2014)
Ann Rheum Dis
   Abstract »    Full Text »
PTPN22 Controls the Germinal Center by Influencing the Numbers and Activity of T Follicular Helper Cells.
C. J. Maine, K. Marquardt, J. Cheung, and L. A. Sherman (2014)
J. Immunol. 192, 1415-1424
   Abstract »    Full Text »    PDF »
Science Signaling Podcast: 27 November 2012.
R. Zamoyska and A. M. VanHook (2012)
Science Signaling 5, pc27
   Abstract »    Full Text »

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