Abstract
The molecular mechanisms explaining why relapses of inflammatory arthritis occur at previously affected sites are unknown. In this issue of Immunity, Friščić et al. propose that local fibroblasts perpetuate inflammation after priming through cell-intrinsic complement C3, which reprograms their bioenergetics and activates the inflammasome.
| Original language | English |
|---|---|
| Journal | Immunity |
| Volume | 54 |
| Issue number | 5 |
| Pages (from-to) | 847-850 |
| Number of pages | 4 |
| ISSN | 1074-7613 |
| DOIs | |
| Publication status | Published - 11.05.2021 |
Funding
This work was supported in part by the Intramural Research Program of the NIH , the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) (project number ZIA/DK075149 to B.A.) and the National Heart, Lung, and Blood Institute (NHLBI) (project number ZIA/Hl006223 to C.K.).
Research Areas and Centers
- Academic Focus: Center for Infection and Inflammation Research (ZIEL)