An NT5E loss-of-function variant permits tissue inflammation and hypertension in systemic lupus erythematosus
Isaac Peabody, Mikhail Olferiev, Katherine A Owen, Tyson Dawson, Prathyusha Bachali, Peter Kasson, Amrie C Grammer, Mary K Crow, Peter E Lipsky · 2026
Read An NT5E loss-of-function variant permits tissue inflammation and hypertension in systemic lupus erythematosus by Isaac Peabody, Mikhail Olferiev, Katherine A Owen, Tyson Dawson, Prathyusha Bachali, Peter Kasson, Amrie C Grammer, Mary K Crow, Peter E Lipsky (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/pmc-13217859.txt.
Description
Isaac Peabody and eight co-authors tied in 2026 a weak variant of the NT5E gene to worse inflammation and high blood pressure in lupus. NT5E makes CD73, an enzyme that produces adenosine, a natural brake on immune attack. The team used systems biology to scan immune and genetic changes in lupus tissue. Signals for making adenosine ran high, yet the calming pathways it feeds ran low.
One variant swaps a single amino acid and was predicted to cripple the enzyme. Carriers showed weaker adenosine control and more cases of heart-lining inflammation and hypertension. The authors say the findings show how a broken brake can let tissue injury proceed. The variant may help explain why some lupus patients develop vascular trouble. It also points to adenosine pathways as targets for future treatment work.
Catalog record
| CREATOR | Isaac Peabody, Mikhail Olferiev, Katherine A Owen, Tyson Dawson, Prathyusha Bachali, Peter Kasson, Amrie C Grammer, Mary K Crow, Peter E Lipsky |
|---|---|
| YEAR | 2026 |
| COLLECTION | PAPERS |
| FORMAT | TXT |
| FILE SIZE | 67 KB |
| VERSION | 1.0 |
| LICENSE | CC BY 4.0 |
| RIGHTS | CC BY |
| SOURCE | Europe PMC |