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See Latest Articlesα9 integrin and its ligands constitute critical joint microenvironments for development of autoimmune arthritis
Journal of Immunology, 06/12/09
Kanayama M et al. - Study provides evidence that the α9 integrin and its ligands (osteopontin and tenascin-C) are critical intrinsic regulators that control the development of autoimmune arthritis, suggesting that the α9 integrin serves as a novel therapeutic target for the treatment of autoimmune disorders, including rheumatoid arthritis (RA).
Methods- Osteopontin (α9 integrin ligand) is critically involved in RA
- However, the molecular cross-talk between osteopontin and joint cell components that leads to the inflammatory joint destruction is largely unknown
- This study examines how OPN and TN-C and their receptor, the α9 integrin, can be integrated into the pathogenesis of arthritis
- OPN, TN-C and their common receptor, α9 integrin, are expressed at arthritic joints
- Local production of OPN and TN-C is mainly due to synovial fibroblasts and, to a lesser extent, synovial macrophages
- Synovial fibroblasts and macrophages express the receptor and its autocrine and paracrine interactions with its ligands on synovial fibroblasts and macrophages contribute differently to the production of proinflammatory cytokines and chemokines
- α9 integrin is also involved in the recruitment and accumulation of inflammatory cells
- Inhibition of α9 integrin function with an anti-α9 integrin Ab significantly reduces the production of arthrogenic cytokines and chemokines and ameliorates ongoing arthritis
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