Revisiting down syndrome through the lens of interferonopathy and innate immune dysregulation
Guangfu Wang, Weili Shi, Shixiu Liao, Bingtao Hao · 2026
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Description
Guangfu Wang and coauthors reframe in 2026 Down syndrome as a condition of interferon-driven immune overactivation, not only a developmental disorder. People with the extra chromosome 21 show chronic inflammation and frequent autoimmune disease. Recent multi-layer studies let the authors connect gene dosage to that immune state.
Extra copies of interferon receptor genes lower the firing threshold of the interferon pathway, keeping defense genes switched on. Reduced chemical tagging of RNA may stabilize inflammatory messages and sharpen innate sensing further. Open chromatin at stress-response sites primes cells to overreact. The authors point to pathway-blocking drugs such as JAK inhibitors as candidate treatments.
Catalog record
| CREATOR | Guangfu Wang, Weili Shi, Shixiu Liao, Bingtao Hao |
|---|---|
| YEAR | 2026 |
| COLLECTION | PAPERS |
| FORMAT | TXT |
| FILE SIZE | 28 KB |
| VERSION | 1.0 |
| LICENSE | CC BY 4.0 |
| RIGHTS | CC BY |
| SOURCE | Europe PMC |