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Sci. Signal., 27 November 2012
Vol. 5, Issue 252, p. pc27
[DOI: 10.1126/scisignal.2003763]


Science Signaling Podcast: 27 November 2012

Rose Zamoyska1 and Annalisa M. VanHook2

1 Institute for Immunology and Infection Research, The University of Edinburgh, West Mains Rd, Edinburgh EH9 3JT UK.
2 Web Editor, Science Signaling, American Association for the Advancement of Science, 1200 New York Avenue, NW, Washington, DC 20005, USA.

Abstract: This Podcast features an interview with Rose Zamoyska, senior author of a Research Article that appears in this issue of Science Signaling. Zamoyska’s group has investigated the role of the protein tyrosine phosphatase PTPN22 in autoimmunity. The balance of immune cell activity is important for keeping the immune system functioning properly, and autoimmune disease can result when effector T cells are overly active or when regulatory T cells, which inhibit effector T cell responses, are less active. PTPN22 has been implicated in autoimmune disease in humans, but mice lacking this phosphatase do not develop spontaneous autoimmunity. The study by Brownlie et al. revealed that, although PTPN22-deficient mice had greater effector T cell activity than wild-type mice, their regulatory T cells also exhibited greater immunosuppressive activity. These findings explain why PTPN22-deficient mice do not develop spontaneous autoimmunity and suggests that PTPN22 could be targeted for treating autoimmune disease.

Citation: R. Zamoyska, A. M. VanHook, Science Signaling Podcast: 27 November 2012. Sci. Signal. 5, pc27 (2012).

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