The Effect of Human Recombinant Tumor Necrosis Factor Receptor-2 on Reducing Inflammatory of Collagen -Induced Arthritis in Balb/c Mice

Background: The tumor necrosis factor alpha (TNF alpha) is a cytokine that produced principally by monocyte/macrophages and T lymphocytes, respectively. TNF alpha is recognized as the primary mediator of immunity in inflammation reaction. One important application of Tumor Necrosis Factor Receptor 2 (TNFR2) is for the treatment of autoimmune diseases like rheumatoid arthritis (RA). Objectives: The aim of this study is to examine the therapeutic trace of the recombinant humanTNFR2 on collagen-induced arthritis (CIA) in mice. Materials and Methods: CIA was created in 20 mice by immunization with bovine type II collagen (CII). After the mice were boosted on day 21, they were injected with the recombinant protein in test group (1 mg.kg(-1)) and assessed edema in paws and knee joints after two weeks. The quantities of inflammatory cytokines such as TNF-alpha, interleukin-1 beta (IL-beta 1), interleukin-6 (IL-6), and interleukin-10(IL-10) in serum were evaluated through enzyme-linked immunosorbent assay (ELISA) kit. In addition, the histopathology of joints sections was analyzed. Results: The cytokines TNF-alpha, IL-1 beta, and IL-6 values in serum markedly decreased in groups treated with TNFR2 (P < 0.01-0.001). The results showed that treatment with TNFR2 significantly reduced edema in paws and joints (P < 0.01-0.001). Conclusions: Pathological investigations proved that administration of recombinant TNF receptor has blocked or protected joints from progressive damage. This study suggests that the anti-arthritic effectiveness of TNFR2 will repress the symptoms of rheumatoid arthritis. Moreover, it seems that TNFR2 is a strong candidate for the treatment of the RA disease.