| First Author | Yue T | Year | 2021 |
| Journal | Science | Volume | 372 |
| Issue | 6543 | PubMed ID | 33986151 |
| Mgi Jnum | J:314967 | Mgi Id | MGI:6713610 |
| Doi | 10.1126/science.aba4220 | Citation | Yue T, et al. (2021) SLFN2 protection of tRNAs from stress-induced cleavage is essential for T cell-mediated immunity. Science 372(6543) |
| abstractText | Reactive oxygen species (ROS) increase in activated T cells because of metabolic activity induced to support T cell proliferation and differentiation. We show that these ROS trigger an oxidative stress response that leads to translation repression. This response is countered by Schlafen 2 (SLFN2), which directly binds transfer RNAs (tRNAs) to protect them from cleavage by the ribonuclease angiogenin. T cell-specific SLFN2 deficiency results in the accumulation of tRNA fragments, which inhibit translation and promote stress-granule formation. Interleukin-2 receptor beta (IL-2Rbeta) and IL-2Rgamma fail to be translationally up-regulated after T cell receptor stimulation, rendering SLFN2-deficient T cells insensitive to interleukin-2's mitogenic effects. SLFN2 confers resistance against the ROS-mediated translation-inhibitory effects of oxidative stress normally induced by T cell activation, permitting the robust protein synthesis necessary for T cell expansion and immunity. |
