IL‐1 is a key cytokine involved in the inflammatory response. The type II receptor of IL‐1 (IL‐1RII) acts as a decoy receptor, binding and inhibiting the effect of IL‐1. This study was undertaken to establish whether IL‐1RII can ameliorate collagen‐induced arthritis, a model of inflammatory arthritis in mice. We used human keratinocytes transfected with the human (h)IL‐1RII gene as a source of hIL‐1RII protein. We showed that these cells expressed both the membrane and soluble form of receptor. In vitro, IL‐1‐stimulated murine macrophage cells showed a decreased expression of TNF‐α in the presence of hIL‐1RII. We engrafted the hIL‐1RII‐transfected cells in the back of mice developing collagen‐induced arthritis. We found that clinical and histological parameters of arthritis were significantly decreased in mice treated with cells producing hIL‐1RII. In addition, hIL‐1RII administration was able to reduce the expression of mRNA for IL‐6 and myeloperoxidase in the joints of treated animals. These data show that hIL‐1RII anti‐inflammatory properties in the model of collagen‐induced arthritis in mice and could have a regulatory role in rheumatoid arthritis.

We explored the possibility that pulsed antigen-presenting cells (APC)

No abstract