Rheumatoid arthritis (RA) is an autoimmune disease characterized by a polyarticular synovitis. In recent years, elderly onset rheumatoid arthritis (EORA) has been increasing. Treg cells in RA have been reported to be dysfunctional, but the relationship between aging and their functional changes is unclear. Here, we found that Treg cells from EORA patients had increased percentages, but decreased activity compared to those from younger onset RA (YORA) patients. In experiments using arthritis model mice, decreased suppressive function and oxygen consumption rate (OCR) were observed in Treg cells only from old arthritic mice. Furthermore, type I interferon (IFN) signaling was upregulated in Treg cells from old GIA mice, and IFN-β decreased the suppressive function of Treg cells. Our findings demonstrate that increased type I IFN signaling in old Treg cells is induced only in the arthritic environment and relates to decreased suppressive function of Treg cells, gets involved in EORA.
Keyphrases
- rheumatoid arthritis
- induced apoptosis
- cell cycle arrest
- end stage renal disease
- chronic kidney disease
- newly diagnosed
- dendritic cells
- disease activity
- oxidative stress
- immune response
- ejection fraction
- signaling pathway
- endoplasmic reticulum stress
- type diabetes
- adipose tissue
- multiple sclerosis
- cell death
- high fat diet induced
- interstitial lung disease
- endothelial cells
- patient reported outcomes
- pi k akt
- patient reported