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Public databases with primary data are ...
  a lot of work
  too much work
  not reliable due to lack of validation
News / MUGEN Network News /
03-06-2009. MUGEN partner Martin Bachmann's group at Cytos Biotechnology shed light to the mechanism of action of Tregs. The researchers show that secreted phospholipase A2 is selectively produced by natural Tregs and acts as a potent suppressor of T cell activation both in vitro and in vivo. The results will be published in the upcoming issue of PNAS
Secretory phospholipase A2-IID is an effector molecule of CD4+ CD25+ regulatory T cells.

Caroline E. von Allmen, Nicole Schmitz, Monika Bauer, Heather J. Hinton, Michael O. Kurrer, Regula B. Buser, Myriam Gwerder, Simone Muntwiler, Roger R. Beerli, and Martin F. Bachmann

Cytos Biotechnology AG, Wagistrasse 25, CH-8952 Schlieren, Switzerland; and Department of Surgical Pathology, University Hospital of Zurich, CH-8091 Zurich, Switzerland

Suppression by natural CD4+ CD25+ regulatory T cells (Tregs) is one mechanism by which tolerance is maintained. However, the way in which Tregs mediate suppression is not well understood. Here, we show that secreted phospholipase A2 (sPLA2)-IID is selectively produced by Tregs. sPLA2-IID is a potent mediator of Treg function, because it strongly suppressed proliferation of CD4+ and CD8+ T cells in vitro and in vivo in a manner independent of its catalytic activity. Furthermore, sPLA2-IID promoted the differentiation of Tregs, presumably via attenuating signaling through the PI3K/Akt/ mammalian target of rapamycin pathway. Importantly, administration of a sPLA2-IID-Fc fusion protein inhibited disease development in murine models of colitis and multiple sclerosis, suggesting that sPLA2-IIDís immunosuppressive function might be exploited therapeutically.
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