Skip to main content

Advertisement

The innate immune system as a therapeutic target in arthritis

Article metrics

  • 876 Accesses

Rheumatoid arthritis is a chronic inflammatory disease that may be characterized by several phases. In the initial induction phase of the disease there may be a breech in the normal mechanisms that protect the host from destruction. In the later phase, pathways that are independent of the adaptive immune system may perpetuate inflammation. These pathways may be active in patients who are refractory to biologic therapies that target key cytokines, IL-1 and tumor necrosis factor alpha. The Toll-like receptors (TLRs) are an integral part of the innate immune system, and are present on synovial lining cells, as well as the cells of the immune system, which may amplify their contribution to the inflammatory cascade. We have found that TLR-4 and its coreceptor CD14 can modulate arthritis and can modulate inflammatory joint disease in murine models of arthritis. In particular, exposure to a TLR-4 ligand stimulates release of IL-6 from synovial fibroblast-like cells in culture, and circumvents the requirement for IL-1 receptor signaling in a serum transfer model of arthritis. These data suggest that triggering the innate immune response through the TLRs with either microbial or autologous ligands plays a role in the initiation or perpetuation of rheumatoid arthritis.

Author information

Rights and permissions

Reprints and Permissions

About this article

Cite this article

Corr, M., Choe, J. & Pekny, K. The innate immune system as a therapeutic target in arthritis. Arthritis Res Ther 5, 135 (2003) doi:10.1186/ar936

Download citation

Keywords

  • Rheumatoid Arthritis
  • Arthritis
  • Tumor Necrosis Factor Alpha
  • Innate Immune System
  • Chronic Inflammatory Disease