| First Author | Ma R | Year | 2024 |
| Journal | Cell Rep | Volume | 43 |
| Issue | 12 | Pages | 115056 |
| PubMed ID | 39645657 | Mgi Jnum | J:361364 |
| Mgi Id | MGI:7852045 | Doi | 10.1016/j.celrep.2024.115056 |
| Citation | Ma R, et al. (2024) Vimentin modulates regulatory T cell receptor-ligand interactions at distal pole complex, leading to dysregulated host response to viral pneumonia. Cell Rep 43(12):115056 |
| abstractText | Forkhead box P3 (Foxp3)(+) regulatory T cells (Tregs) resolve acute inflammation and repair the injured lung after viral pneumonia. Vimentin is a critical protein in the distal pole complex (DPC) of Tregs. This study reveals the inhibitory effect of vimentin on the suppressive and reparative capacity of Tregs. Treg-specific deletion of vimentin increases Helios(+)interleukin-18 receptor (IL-18R)(+) Tregs, suppresses inflammatory immune cells, and enhances tissue repair, protecting Vim(fl/fl)Foxp3(YFP-cre) mice from influenza-induced lung injury and mortality. Mechanistically, vimentin suppresses the induction of amphiregulin, an epidermal growth factor receptor (EGFR) ligand necessary for tissue repair, by sequestering IL-18R to the DPC and restricting receptor-ligand interactions. We propose that vimentin in the DPC of Tregs functions as a molecular switch, which could be targeted to regulate the immune response and enhance tissue repair in patients with severe viral pneumonia. |
