Elevated ST2+ Tregs in RA-ILD: correlation with pulmonary fibrosis and the IL-33/ST2/amphiregulin (AREG) axis
Authors' conclusion
These results highlight the potential involvement of the IL-33/ST2 axis in mediating a pathogenic Tregs response characterized by AREG production, thereby linking systemic autoimmunity to the progression of lung fibrosis in RA-ILD.
Study context
- Population
- Clinical cohort of healthy controls, rheumatoid arthritis (RA) patients without interstitial lung disease (ILD) and RA patients with ILD; composite collagen-induced arthritis (CIA) + bleomycin (BLM) murine model
- Comparison
- RA-ILD vs RA-nonILD vs healthy controls; CIA + BLM mice
- Outcome
- Role of ST2+ Tregs in the progression of RA-ILD
Methodological detailscomposite murine model (CIA + intratracheal BLM), clinical cohort, flow cytometry, AI-based quantitative high-resolution computed tomography (HRCT) analysis, in vitro studies
- Composite murine model (CIA + intratracheal BLM)
- Clinical cohort
- Flow cytometry
- AI-based quantitative HRCT analysis
- In vitro studies
Main finding
As reported in the abstract
- Composite model exhibited exacerbated lung inflammation and fibrosis (histopathology)
- Marked expansion of ST2+ Tregs in lungs of CIA + BLM mice and peripheral blood of RA-ILD patients
- Positive correlation between ST2+ Treg frequency and fibrotic lung volume on quantitative HRCT
- Elevated serum IL-33 and AREG in RA-ILD patients, correlated with disease severity
- IL-33 stimulation significantly upregulated AREG mRNA and protein in Tregs in vitro
Original publication
Elevated ST2+ Tregs in RA-ILD: correlation with pulmonary fibrosis and the IL-33/ST2/AREG axis. Arthritis Res Ther. Published 28 May 2026. doi:10.
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