Effect of tumor necrosis factor receptor-2 in reduction of arthritis severity in balb/c mice

Shahla Korani,1,*



Rheumatoid arthritis (ra) is one of the most common forms of inflammatory arthritis, causing suffering, disability and even premature death. many of the past and current therapies offer little more than symptomatic relief. the most common treatments for rheumatoid arthritis include nonsteroidal anti-inflammatory drugs (nsaids), corticosteroids, disease modifying antirheumatic drugs (dmards), and some biological agents. tumour necrosis factor (tnf) is a pro-inflammatory cytokine that signals through two distinct receptors, tnfr1 and tnfr2. tnfr is involved in the pathogenesis of various inflammatory. blocking tnf, in turn, has been showed to be highly effective in treating autoimmune diseases. the aim of this study is to investigate the protective effect of the tnfr2 on collagen-induced arthritis in mice.


Collagen-induced arthritis )cia( was induced in mice by immunization with bovine typeii collagen(ii).after boosted on day21,mice were treated with tnfr2and mtx(1mg/kg)for twelve consecutive days. the clinical scores and joint histopathology were evaluated.


Administration of tnfr2 significantly protected ankle bone and cartilage from being eroded versus disease mice. pathological examination showed that tnfr2 effectively reduced inflammation severity in cia.


In this present study, it is demonstrated that administration of tnfr2 has potential and therapeutic effect on cia. the data suggests that tnfr2 could have a role in improved management of ra patients.


Collagen-induced arthritis, rheumatoid arthritis, tumour necrosis factor, tnfr2