| First Author | Inoue M | Year | 2018 |
| Journal | Nat Immunol | Volume | 19 |
| Issue | 11 | Pages | 1265-1276 |
| PubMed ID | 30323341 | Mgi Jnum | J:282664 |
| Mgi Id | MGI:6381326 | Doi | 10.1038/s41590-018-0222-z |
| Citation | Inoue M, et al. (2018) Arginine methylation controls the strength of gammac-family cytokine signaling in T cell maintenance. Nat Immunol 19(11):1265-1276 |
| abstractText | The methylation of arginine residues in proteins is a post-translational modification that contributes to a wide range of biological processes. Many cytokines involved in T cell development and activation utilize the common cytokine receptor gamma-chain (gammac) and the kinase JAK3 for signal transduction, but the regulatory mechanism that underlies the expression of these factors remains unclear. Here we found that the arginine methyltransferase PRMT5 was essential for the maintenance of invariant natural killer T cells (iNKT cells), CD4(+) T cells and CD8(+) T cells. T cell-specific deletion of Prmt5 led to a marked reduction in signaling via gammac-family cytokines and a substantial loss of thymic iNKT cells, as well as a decreased number of peripheral CD4(+) T cells and CD8(+) T cells. PRMT5 induced the symmetric dimethylation of Sm proteins that promoted the splicing of pre-mRNA encoding gammac and JAK3, and this critically contributed to the expression of gammac and JAK3. Thus, arginine methylation regulates strength of signaling via gammac-family cytokines by facilitating the expression of signal-transducing components. |
