Rheumatoid arthritis is a chronic inflammatory disease characterized by joint destruction and the proliferation of synovium. It has been suggested that the extracellular matrix protein osteopontin (OPN) may facilitate this destruction, but the molecular mechanisms involved have been unclear. In the July 15 Journal of Clinical Investigation, Nobuchika Yamamoto and colleagues at the Fujisawa Pharmaceutical Company show that a cryptic epitope, the SLAYGLR sequence of murine OPN, is critically involved in the pathogenesis of inflammatory arthritis and associated joint destruction (Journal of Clinical Investigation, 112:181-188, July 15, 2003).

Yamamoto et al. examined splenic monocytes from a murine model of rheumatoid arthritic mice. They observed that the M5 antibody—specific for the SLAYGLR sequence of murine OPN—abrogated monocyte migration toward the thrombin-cleaved form of OPN. In addition, they showed that M5 inhibited the proliferation of synovium, bone erosion, and inflammatory cell infiltration in arthritic joints.

"The study of Yamamoto...

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