Protection of human endothelial cells against complement-mediated lycls 3135 Relative roles of decay-accelerating factor, membrane cofactor protein, and CD59 in the protection of human endothelial cells against complement-mediated lysis\* Human umbilical vein endothelial cells (HUVEC) were found b
The effects of functional suppression of a membrane-bound complement regulatory protein, CD59, in the synovial tissue in rats
โ Scribed by Masashi Mizuno; Kazuhiro Nishikawa; Rhian M. Goodfellow; Sara J. Piddlesden; B. Paul Morgan; Seiichi Matsuo; Seiichi Matsuo
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 688 KB
- Volume
- 40
- Category
- Article
- ISSN
- 0004-3591
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โฆ Synopsis
Objective. To investigate the roles of CD59 in the synovial tissue by functional suppression of CD59.
Methods. Rats treated with cobra venom factor to deplete complement or untreated rats were injected intraarticularly with 0.3 mg of the F(ab'), fraction of a monoclonal antibody, 6D1, that inhibits the function of rat CD59. The circumference of knee joints was measured, and histologic changes in the synovium were studied.
Results. Joint swelling, thickening of the synovial tissues, infiltration of inflammatory cells into the synovium, and deposition of membrane attack complex (MAC) on the synovial surface were observed after intraarticular injection of 6D1. The inflammatory reaction reached its peak at 24 hours after injection, and finally subsided to normal within 3 days. It was suggested that functional suppression of CD59 in the synovium induced MAC formation followed by synovitis. Serum complement depletion did not completely suppress this reaction. This indicates that complement existing in the joint space is important for the formation of MAC on the synovial surface and for induction of synovitis.
Conclusion. The membrane-bound complement regulatory protein, CD59, plays a key role in the protection of joints against MAC-mediated synovial injury and in maintaining the normal integrity of the joint.
The membrane attack complex (MAC; C5b-9) is known to trigger the synthesis and release of various
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