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Updated: Sep 18, 2025

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Zijun Ma1, Na Zheng2, Yingying Wei3
1Department of Rheumatology, Fujian Institute of Clinical Immunology, Fujian Medical University Union Hospital; Department of Rheumatology and Immunology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology.
Abstract:
Rheumatoid arthritis (RA) is a chronic, systemic autoimmune inflammatory disorder that may result in joint damage, deformities, disability, and even death. Due to its complex etiology and heterogeneous clinical presentation, current treatment strategies remain inadequate in effectively controlling disease progression, particularly in achieving early diagnosis and providing personalized therapies. Therefore, developing novel therapeutic approaches is crucial. To achieve this, reliable animal models are essential for investigating the pathogenesis of RA. Currently, several animal models of RA are used, including the collagen-induced arthritis model (CIA), the K/BxN model, and the SKG mouse. Although these models can successfully mimic the immune mechanisms and clinical manifestations of RA, they each have notable limitations. In this protocol, we describe the process of establishing an RA mouse model through the adoptive transfer of CD4+ T cells from SKG mice. Compared to conventional models, this model offers a shorter establishment time and a higher incidence rate (100%) in C57BL/6 mice. It is relatively cost-effective, involves straightforward procedures, and reliably replicates T-cell-mediated immune responses, ensuring superior experimental control and reproducibility. We conducted a comprehensive evaluation of the model, assessing the clinical phenotype such as joint symptoms. Through clinical phenotype assessment, we observed significant joint swelling and inflammatory responses. Additionally, using PCR technology to measure the expression levels of key transcription factors, we found that this model effectively simulates T cell-mediated immune responses and key pathological features of RA. With this model, researchers can better simulate the T cell-mediated immune response and key pathological features of RA, thus providing a reliable and effective experimental tool for studying immune mechanisms and pathological progression and developing novel therapies for RA.
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