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Immune Aging in Rheumatoid Arthritis.
Cornelia M Weyand1, Jörg J Goronzy1
1Mayo Clinic Alix School of Medicine, Mayo Clinic College of Medicine and Science, Rochester, Minnesota, and Stanford University School of Medicine, Stanford, California.
Rheumatoid arthritis (RA) is linked to premature immune aging, where aged T cells and B cells drive inflammation and autoimmunity. This accelerated aging process precedes joint inflammation in RA patients.
Area of Science:
- Immunology
- Gerontology
- Rheumatology
Background:
- Rheumatoid arthritis (RA) is a chronic autoimmune disease influenced by genetics and environment.
- RA incidence increases with age, suggesting a role for the aging process in disease susceptibility.
Purpose of the Study:
- To explore the relationship between immune aging and rheumatoid arthritis (RA) risk.
- To elucidate mechanisms by which immune aging contributes to autoimmunity in RA.
Main Methods:
- Review of molecular immunology and functional genomics findings.
- Analysis of T cell, B cell, and myeloid cell aging signatures in RA.
Main Results:
- Patients with RA exhibit premature immune aging, particularly in CD4+ T cells.
- Accelerated immune aging, characterized by cellular and organelle dysfunction, precedes joint inflammation.
- Age-associated B cells and aged myeloid cells contribute to RA pathogenesis and inflammaging.
Conclusions:
- Premature immune aging is a significant factor in RA development and progression.
- Dysfunctional immune cells, driven by aging processes, promote chronic inflammation and autoimmunity in RA.
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