期刊
JOURNAL OF IMMUNOLOGY
卷 186, 期 7, 页码 4361-4366出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1002857
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资金
- National Institutes of Health [P01 AI065858]
- Arthritis Foundation
- Cogan Family Foundation
- British Heart Foundation
- National Heart, Lung, and Blood Institute [HL50545]
- MRC [G0400701] Funding Source: UKRI
- British Heart Foundation [RG/09/003/27122] Funding Source: researchfish
- Medical Research Council [G0400701] Funding Source: researchfish
In addition to the well-described role of platelets in thrombosis, a growing body of evidence implicates platelets in diverse inflammatory responses. We recently showed platelets can contribute to the pathophysiology of inflammatory arthritis via IL-1-containing microparticles. In this study, we demonstrate that platelets, and not platelet microparticles, actively contribute to synovitis via production of proinflammatory prostacyclin in an autoimmune arthritis model. Using both genetic and pharmacologic approaches, we establish that paracrine production of prostacyclin proceeds in the absence of cyclooxygenase-2. Furthermore, we also demonstrate that prostacyclin generation can arise via transcellular collaboration between platelets and fibroblast-like synoviocytes. In addition to shedding light on an unappreciated pathway of lipid synthesis in arthritis, we further delineate a novel effector activity by which platelets can contribute to inflammatory disease. The Journal of Immunology, 2011, 186: 4361-4366.
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