دوره 2، شماره 3 - ( 7-1402 )
جلد 2 شماره 3 صفحات 67-59 |
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Bagherifar F, Tavassoli Razavi F, Ghoryani M. Regulatory T Cell Plasticity in Rheumatoid Arthritis: Mechanisms, Pathogenic Roles, and Therapeutic Implications. Journal title 2023; 2 (3) :59-67
URL: http://jrhms.thums.ac.ir/article-1-97-fa.html
URL: http://jrhms.thums.ac.ir/article-1-97-fa.html
انعطافپذیری سلولهای T تنظیمکننده در آرتریت روماتوئید: مکانیسمها، نقشهای بیماریزا و پیامدهای درمانی. عنوان نشریه. 1402; 2 (3) :59-67
چکیده: (7 مشاهده)
Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by persistent inflammation, progressive joint damage, and functional disability. The plasticity of regulatory T cells (Tregs) plays a central role in the immunopathogenesis of RA by disrupting immune tolerance and promoting pro-inflammatory T helper (Th) 17 (Th17)-like responses. In this review, a comprehensive literature search was conducted in the PubMed, Scopus, and Web of Science databases up to May 2025, using the keywords “rheumatoid arthritis,” “regulatory T cells,” “regulatory T Cell plasticity,” and “immune system regulation.” Reference lists of retrieved publications were manually screened to identify additional relevant studies. Priority was given to peer-reviewed experimental and clinical studies addressing Treg biology, molecular mechanisms of plasticity, and therapeutic implications. Only English-language articles were included, and quality was assessed based on study design, sample size, and reproducibility of findings. Evidence indicates that inflammatory cytokines, metabolic alterations, and epigenetic reprogramming disrupt the stability of forkhead box protein 3 (Foxp3) and promote the conversion of Tregs into Th17- like cells. This shift diminishes suppressive capacity and increases interleukin (IL) 17 (IL-17) production, thereby exacerbating synovial inflammation and joint destruction. Clinical data demonstrate that unstable Foxp3+RORγt+ Tregs correlate with disease activity and radiographic progression in RA. Current therapeutic strategies—including IL-6 receptor inhibitors, Janus kinase (JAK) inhibitors, rapamycin, and epigenetic modulators—show potential in preserving Treg stability. Moreover, emerging approaches such as chimeric antigen receptor (CAR)-Treg cells and microRNA-based interventions represent innovative directions for targeted immunotherapy. Treg plasticity plays a pivotal role in the pathogenesis of RA and offers novel opportunities for therapeutic intervention. Stabilizing Treg identity and preventing their pathological conversion have the potential to restore immune tolerance, reduce inflammation, and halt disease progression. Clinicians could consider the implications of Treg-targeted strategies as adjuncts to conventional immunomodulatory therapies.
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