| First Author | Siegmund K | Year | 2017 |
| Journal | PLoS One | Volume | 12 |
| Issue | 5 | Pages | e0175463 |
| PubMed ID | 28531229 | Mgi Jnum | J:246450 |
| Mgi Id | MGI:5914835 | Doi | 10.1371/journal.pone.0175463 |
| Citation | Siegmund K, et al. (2017) Protein kinase C theta is dispensable for suppression mediated by CD25+CD4+ regulatory T cells. PLoS One 12(5):e0175463 |
| abstractText | The activation of conventional T cells upon T cell receptor stimulation critically depends on protein kinase C theta (PKCtheta). However, its role in regulatory T (Treg) cell function has yet to be fully elucidated. Using siRNA or the potent and PKC family-selective pharmacological inhibitor AEB071, we could show that murine Treg-mediated suppression in vitro is independent of PKCtheta function. Likewise, Treg cells of PKCtheta-deficient mice were fully functional, showing a similar suppressive activity as wild-type CD25+CD4+ T cells in an in vitro suppression assay. Furthermore, in vitro-differentiated wild-type and PKCtheta-deficient iTreg cells showed comparable Foxp3 expression as well as suppressive activity. However, we observed a reduced percentage of Foxp3+CD25+ CD4+ T cells in the lymphatic organs of PKCtheta-deficient mice. Taken together, our results suggest that while PKCtheta is involved in Treg cell differentiation in vivo, it is dispensable for Treg-mediated suppression. |
