REGULATORY T (Treg) cells are vital for immune system balance, preventing autoimmune diseases by suppressing inflammation. Yet in inflammatory arthritis, these cells often accumulate in inflamed joints without alleviating the condition. This contradiction, termed the “Treg paradox,” underscores their complex role in arthritis pathogenesis.
Research highlights that while Treg cells are abundant in arthritis-affected joints, their ability to suppress inflammation is compromised. Factors such as genetic variants, inflammatory cytokines, and oxygen-deprived environments constrain Treg cell function. Moreover, Treg cells can undergo harmful transformations, becoming pro-inflammatory or contributing to tissue damage by releasing molecules like RANKL.
This discovery reframes the understanding of arthritis as not merely a failure of Treg cells but also a case where these immune regulators exacerbate the disease. Current disease-modifying antirheumatic drugs (DMARDs) may partially restore Treg cell function, and emerging treatments aim to harness these cells therapeutically.
The findings provide a roadmap for targeting Treg cells to combat inflammatory arthritis. With novel interventions under development, addressing the Treg paradox could usher in a new era of personalized, immune-based therapies for patients suffering from chronic joint inflammation.
This research reveals not just the challenges but also the untapped potential of Treg-directed treatments, offering hope for more effective arthritis management strategies.
Reference: Schnell JT et al. The ‘Treg paradox’ in inflammatory arthritis. Nat Rev Rheumatol (2024). doi: 10.1038/s41584-024-01190-w.
Anaya Malik | AMJ
