Rheumatoid Arthritis (RA) is an autoimmune disease characterized by inflammation and eventual destruction of the synovial joints. The role of platelets in the pathophysiology of arthritis has only recently been established. Because antibodies to CD44 can deplete platelets, we hypothesized that these antibodies might be effective in arthritis through a platelet-depletion mechanism. We examined the K/BxN passive transfer mouse model of arthritis and found that most antibodies against CD44 were capable of depleting platelets. However, anti-CD44 treatment is effective when administered during developing arthritis, while anti-platelet treatment was not. While CD44 antibodies may be therapeutic through platelet-dependant and independent mechanisms, the ability of CD44 antibodies to decrease platelet counts does not seem to be the critical factor in resolving arthritis in the K/BxN model.
| Identifer | oai:union.ndltd.org:TORONTO/oai:tspace.library.utoronto.ca:1807/33465 |
| Date | 26 November 2012 |
| Creators | Mott, Patrick Joseph |
| Contributors | Lazarus, Alan H. |
| Source Sets | University of Toronto |
| Language | en_ca |
| Detected Language | English |
| Type | Thesis |
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