Rheumatoid Arthritis Model

Introduction

Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease characterized by symmetric joint inflammation and polyarticular involvement, often leading to joint pain, swelling, and functional impairment. Joint damage in this condition is typically caused by the interplay of cytokines, chemokines, and metalloproteinases. Typical manifestations of RA include symmetric peripheral polyarthritis, particularly in the wrists and finger joints, which undergo persistent structural damage and may be accompanied by systemic symptoms.

Disease models

The SMOC has long been dedicated to autoimmune disease research and has developed a variety of rheumatoid arthritis mouse models, providing powerful tools for the efficacy evaluation and safety assessment of related drugs.

Using a collagen‑induced rheumatoid arthritis model in DBA mice, the groups were divided into a blank control group (Control), a chicken collagen model group (Chicken II), a treatment group of the chicken collagen model (Chicken II + Dex), a bovine collagen model group (Bovine II), and a treatment group of the bovine collagen model (Bovine II + Dex).

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Fig.1 Clinical score of CII-induced rheumatoid arthritis. (A) the onset mouse symptoms. (B) The body weight. (C) clinical score of rheumatoid arthritis by chicken CII and bovine CII induction and dexamethasone treatment. Red arrow means swollen of the joints.

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Fig.2 Representative micro-computerized tomography (CT) images of the onset mouse bone symptoms.

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Fig.3 The results of H&E and Safranin O fast green stain. (A) Representative images of HE and Safranin O fast green stain. (B) Histopathology score. *** P<0.001 vs Group 1, ### P<0.001 vs Group 3.Blue arrow means Joint fibrosis. Red arrow means inflammatory cell infiltration. Black arrow means cartilage damaged.

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Fig.1 Efficacy of Sirukumab in hIL6/hIL6R mice in collagen-induced arthritis (CIA) model. Group 1 received no immunization. Group 2 were immunized to induce CIA. Group 3 were immunized to induce CIA and treated with Sirukumab. Body weight was monitored throughout the study and remained stable across all groups (A). After CIA induction, clinical score increase, indicating successful model establishment. Mice treated with Sirukumab exhibited reduction in arthritis severity as evidenced by decreased clinical scores (B). Data are presented as mean ± SEM(n=10-15).

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Fig.2 Efficacy of Sirukumab in hIL6/hIL6R mice in collagen-induced arthritis (CIA) model. Group 1 received no immunization. Group 2 were immunized to induce CIA. Group 3 were immunized to induce CIA and treated with Sirukumab. Representative diagram of hind limb joints of mice in each group at the end of the study. 

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Fig.3 Gross pathology and relative weight of spleen each group in collagen-induced arthritis (CIA) model in hIL6hIL6R mice. Group 1 received no immunization. Group 2 were immunized to induce CIA. Group 3 were immunized to induce CIA and treated with Sirukumab. Data are presented as mean ± SEM (n=10-15).

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Fig.4 Gross pathology and relative weight of kidney each group in collagen-induced arthritis (CIA) model in hIL6hIL6R mice. Group 1 received no immunization. Group 2 were immunized to induce CIA. Group 3 were immunized to induce CIA and treated with Sirukumab. Data are presented as mean ± SEM (n=10-15).

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Fig.5 Representative micro-CT images of ankle joint of each group in collagen-induced arthritis (CIA) model in hIL6hIL6R mice. Group 1 received no immunization. Group 2 were immunized to induce CIA. Group 3 were immunized to induce CIA and treated with Sirukumab.

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