| First Author | Lawless SJ | Year | 2017 |
| Journal | Nat Commun | Volume | 8 |
| Pages | 15620 | PubMed ID | 28555668 |
| Mgi Jnum | J:249557 | Mgi Id | MGI:5921395 |
| Doi | 10.1038/ncomms15620 | Citation | Lawless SJ, et al. (2017) Glucose represses dendritic cell-induced T cell responses. Nat Commun 8:15620 |
| abstractText | Glucose and glycolysis are important for the proinflammatory functions of many immune cells, and depletion of glucose in pathological microenvironments is associated with defective immune responses. Here we show a contrasting function for glucose in dendritic cells (DCs), as glucose represses the proinflammatory output of LPS-stimulated DCs and inhibits DC-induced T-cell responses. A glucose-sensitive signal transduction circuit involving the mTOR complex 1 (mTORC1), HIF1alpha and inducible nitric oxide synthase (iNOS) coordinates DC metabolism and function to limit DC-stimulated T-cell responses. When multiple T cells interact with a DC, they compete for nutrients, which can limit glucose availability to the DCs. In such DCs, glucose-dependent signalling is inhibited, altering DC outputs and enhancing T-cell responses. These data reveal a mechanism by which T cells regulate the DC microenvironment to control DC-induced T-cell responses and indicate that glucose is an important signal for shaping immune responses. |
