Related Experiment Video
Updated: Jun 23, 2026
07:37
An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
Adiposity-Associated Monocyte Costimulatory Programming in Rheumatoid Arthritis Identified by Single-Cell
Shalini N Swamy1, Hua Zhong2, Kylie Williams3
1Section of Rheumatology, Allergy and Immunology, Department of Medicine, College of Medicine, University of Oklahoma Health Sciences, Oklahoma City, OK, USA.
Medrxiv : the Preprint Server for Health Sciences
|June 22, 2026
Summary
Obesity amplifies immune activation in rheumatoid arthritis (RA) by enhancing monocyte costimulatory pathways. This metabolic dysregulation may worsen RA disease activity and outcomes.
Area of Science:
- Immunology
- Rheumatology
- Metabolic disease
Background:
- Rheumatoid arthritis (RA) is a chronic inflammatory disease with significant morbidity.
- Obesity is linked to increased RA disease activity and poorer long-term outcomes.
- Understanding the link between adiposity and immune dysregulation is crucial for refining RA treatments.
Purpose of the Study:
- To investigate how adiposity influences monocyte programming in rheumatoid arthritis.
- To determine if obesity enhances monocyte costimulatory signaling, promoting adaptive immune activation in RA.
Main Methods:
- Single-cell RNA sequencing of circulating monocytes from 16 RA patients and 15 controls.
- Analysis of transcriptomic profiles to identify monocyte populations and pathway enrichment.
- Statistical evaluation of associations between disease status, body mass index (BMI), and immune activation pathways.
Main Results:
- RA monocytes showed enrichment in antigen processing and presentation pathways.
- Higher BMI in RA patients correlated with increased enrichment of T-cell costimulatory pathways.
- Specific costimulatory molecules (CD86, ICOSLG, TNFSF4) showed patterns consistent with inducible signaling.
Conclusions:
- Metabolic dysregulation, particularly obesity, amplifies monocyte-mediated immune activation in RA.
- This amplified immune activation may contribute to more severe RA disease activity and outcomes.
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