| First Author | Blagih J | Year | 2015 |
| Journal | Immunity | Volume | 42 |
| Issue | 1 | Pages | 41-54 |
| PubMed ID | 25607458 | Mgi Jnum | J:263540 |
| Mgi Id | MGI:6141580 | Doi | 10.1016/j.immuni.2014.12.030 |
| Citation | Blagih J, et al. (2015) The energy sensor AMPK regulates T cell metabolic adaptation and effector responses in vivo. Immunity 42(1):41-54 |
| abstractText | Naive T cells undergo metabolic reprogramming to support the increased energetic and biosynthetic demands of effector T cell function. However, how nutrient availability influences T cell metabolism and function remains poorly understood. Here we report plasticity in effector T cell metabolism in response to changing nutrient availability. Activated T cells were found to possess a glucose-sensitive metabolic checkpoint controlled by the energy sensor AMP-activated protein kinase (AMPK) that regulated mRNA translation and glutamine-dependent mitochondrial metabolism to maintain T cell bioenergetics and viability. T cells lacking AMPKalpha1 displayed reduced mitochondrial bioenergetics and cellular ATP in response to glucose limitation in vitro or pathogenic challenge in vivo. Finally, we demonstrated that AMPKalpha1 is essential for T helper 1 (Th1) and Th17 cell development and primary T cell responses to viral and bacterial infections in vivo. Our data highlight AMPK-dependent regulation of metabolic homeostasis as a key regulator of T cell-mediated adaptive immunity. |
