| First Author | Douguet L | Year | 2016 |
| Journal | PLoS One | Volume | 11 |
| Issue | 11 | Pages | e0165639 |
| PubMed ID | 27812136 | Mgi Jnum | J:250669 |
| Mgi Id | MGI:6099903 | Doi | 10.1371/journal.pone.0165639 |
| Citation | Douguet L, et al. (2016) Nitric Oxide Synthase 2 Improves Proliferation and Glycolysis of Peripheral gammadelta T Cells. PLoS One 11(11):e0165639 |
| abstractText | gammadelta T cells play critical roles in host defense against infections and cancer. Although advances have been made in identifying gammadelta TCR ligands, it remains essential to understand molecular mechanisms responsible for in vivo expansion of gammadelta T cells in periphery. Recent findings identified the expression of the inducible NO synthase (NOS2) in lymphoid cells and highlighted novel immunoregulatory functions of NOS2 in alphabeta T cell differentiation and B cell survival. In this context, we wondered whether NOS2 exerts an impact on gammadelta T cell properties. Here, we show that gammadelta T cells express NOS2 not only in vitro after TCR triggering, but also directly ex vivo. Nos2 deficient mice have fewer gammadelta T cells in peripheral lymph nodes (pLNs) than their wild-type counterparts, and these cells exhibit a reduced ability to produce IL-2. Using chemical NOS inhibitors and Nos2 deficient gammadelta T cells, we further evidence that the inactivation of endogenous NOS2 significantly reduced gammadelta T cell proliferation and glycolysis metabolism that can be restored in presence of exogenous IL-2. Collectively, we demonstrate the crucial role of endogenous NOS2 in promoting optimal IL-2 production, proliferation and glycolysis of gammadelta T cells that may contribute to their regulation at steady state. |
