2010 January 29; 327(5965): 580–583 | Eric Boillard, Peter A. Nigrovic, Katherine Larabee, Gerald F. M. Watts, Jonathan S. Coblyn, Michael E. Weinblatt, Elena M. Massarotti, Eileen Remold-O'Donnell, Richard W. Farndale, Jerry Ware, and David M. Lee
This study investigates the role of platelets in rheumatoid arthritis (RA) and other inflammatory arthritides. Platelet microparticles (MPs), submicrometer vesicles produced by activated platelets, were found to be abundant in joint fluid from patients with RA and other inflammatory arthritides but not in osteoarthritis patients. These MPs were proinflammatory, eliciting cytokine responses from synovial fibroblasts via interleukin-1 (IL-1). Depletion of platelets in mice attenuated inflammatory arthritis. The collagen receptor glycoprotein VI (GPVI) was identified as a key trigger for platelet MPs in arthritis pathophysiology. Platelet MPs likely contribute to joint inflammation through mechanisms including IL-1-mediated activation of synoviocytes. These findings highlight a previously unappreciated role for platelets and their MPs in inflammatory joint diseases.This study investigates the role of platelets in rheumatoid arthritis (RA) and other inflammatory arthritides. Platelet microparticles (MPs), submicrometer vesicles produced by activated platelets, were found to be abundant in joint fluid from patients with RA and other inflammatory arthritides but not in osteoarthritis patients. These MPs were proinflammatory, eliciting cytokine responses from synovial fibroblasts via interleukin-1 (IL-1). Depletion of platelets in mice attenuated inflammatory arthritis. The collagen receptor glycoprotein VI (GPVI) was identified as a key trigger for platelet MPs in arthritis pathophysiology. Platelet MPs likely contribute to joint inflammation through mechanisms including IL-1-mediated activation of synoviocytes. These findings highlight a previously unappreciated role for platelets and their MPs in inflammatory joint diseases.