Science. 2010 January 29; 327(5965): 580–583. doi:10.1126/science.1181928

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Eric Boilard1, Peter A. Nigrovic1,2, Katherine Larabee1, Gerald F. M. Watts1, Jonathan S.
Coblyn1, Michael E. Weinblatt1, Elena M. Massarotti1, Eileen Remold-O’Donnell3, Richard
W. Farndale4, Jerry Ware5, and David M. Lee1,*
1Division of Rheumatology, Immunology and Allergy, Brigham and Women’s Hospital, Harvard
Medical School, Boston, MA 02115, USA
2Division of Immunology, Children’s Hospital Boston, Boston, MA 02115, USA
3Immune Disease Institute, Harvard Medical School, Boston MA 02115, USA
4University of Cambridge, Department of Biochemistry, Downing Site, Cambridge CB2 1QW, UK
5University of Arkansas for Medical Sciences, Little Rock, AR 72205–7199, USA


In addition to their pivotal role in thrombosis and wound repair, platelets participate in inflammatory responses. We investigated the role of platelets in the autoimmune disease rheumatoid arthritis. We identified platelet microparticles—submicrometer vesicles elaborated by activated platelets—in joint fluid from patients with rheumatoid arthritis and other forms of inflammatory arthritis, but not in joint fluid from patients with osteoarthritis. Platelet microparticles were proinflammatory, eliciting cytokine responses from synovial fibroblasts via interleukin-1. Consistent with these findings, depletion of platelets attenuated murine inflammatory arthritis. Using both pharmacologic and genetic approaches, we identified the collagen receptor glycoprotein VI as a key trigger for platelet microparticle generation in arthritis pathophysiology. Thus, these findings demonstrate a previously unappreciated role for platelets and their activation-induced microparticles in inflammatory joint diseases.