| First Author | Yarosz EL | Year | 2020 |
| Journal | J Immunol | Volume | 204 |
| Issue | 7 | Pages | 1708-1713 |
| PubMed ID | 32122995 | Mgi Jnum | J:287586 |
| Mgi Id | MGI:6406010 | Doi | 10.4049/jimmunol.1901399 |
| Citation | Yarosz EL, et al. (2020) Cutting Edge: Activation-Induced Iron Flux Controls CD4 T Cell Proliferation by Promoting Proper IL-2R Signaling and Mitochondrial Function. J Immunol 204(7):1708-1713 |
| abstractText | Iron has long been established as a critical mediator of T cell development and proliferation. However, the mechanisms by which iron controls CD4 T cell activation and expansion remain poorly understood. In this study, we show that stimulation of CD4 T cells from C57BL/6 mice not only decreases total and labile iron levels but also leads to changes in the expression of iron homeostatic machinery. Additionally, restraining iron availability in vitro severely inhibited CD4 T cell proliferation and cell cycle progression. Although modulating cellular iron levels increased IL-2 production by activated T lymphocytes, CD25 expression and pSTAT5 levels were decreased, indicating that iron is necessary for IL-2R-mediated signaling. We also found that iron deprivation during T cell stimulation negatively impacts mitochondrial function, which can be reversed by iron supplementation. In all, we show that iron contributes to activation-induced T cell expansion by positively regulating IL-2R signaling and mitochondrial function. |
