IL-17–driven transcriptional programs in muscle fibroblasts are not required for pathogenesis in murine anti-histidyl-tRNA synthetase (Jo-1) myositis
Decheng Li, Daniel P Reay, Yang Li, Shachi P Vyas, Kenta Yamamoto, Dana P Ascherman, Sarah L Gaffen · 2026
Read IL-17–driven transcriptional programs in muscle fibroblasts are not required for pathogenesis in murine anti-histidyl-tRNA synthetase (Jo-1) myositis by Decheng Li, Daniel P Reay, Yang Li, Shachi P Vyas, Kenta Yamamoto, Dana P Ascherman, Sarah L Gaffen (2026) in the Tower of Babel, a free online library of public-domain works preserved in clean, searchable text. No sign-up. The full text is served as a plain-text file at a predictable URL, where text is present: https://antarctic-labs.com/tower-of-babel/PMC13439884.txt.
Description
Li and colleagues test whether an inflammatory signal drives muscle disease in a mouse model of myositis in this 2026 study. Myositis is an autoimmune attack on muscle, and the Jo-1 form targets a specific enzyme. The team profiled muscle fibroblasts with single-cell sequencing. Fibroblasts are support cells that orchestrate inflammation. A strong IL-17 gene program was switched on during disease. It included a coactivator called IκBζ.
In dishes, IL-17 potently activated IκBζ in fibroblasts, and the coactivator was essential for the cells to respond to IL-17 at all. Yet removing the pathway in living mice changed nothing about the disease: tissue inflammation and autoantibody production proceeded as usual. The authors conclude that a loud molecular signature is not necessarily a driver, a caution for choosing drug targets in myositis.
Catalog record
| CREATOR | Decheng Li, Daniel P Reay, Yang Li, Shachi P Vyas, Kenta Yamamoto, Dana P Ascherman, Sarah L Gaffen |
|---|---|
| YEAR | 2026 |
| COLLECTION | PAPERS |
| FORMAT | TXT |
| FILE SIZE | 38 KB |
| LICENSE | https://creativecommons.org/licenses/by/4.0 |
| RIGHTS | CC BY |
| SOURCE | Europe PMC |