| First Author | Yang YH | Year | 2001 |
| Journal | J Immunol | Volume | 167 |
| Issue | 2 | Pages | 1047-52 |
| PubMed ID | 11441114 | Mgi Jnum | J:120523 |
| Mgi Id | MGI:3706726 | Doi | 10.4049/jimmunol.167.2.1047 |
| Citation | Yang YH, et al. (2001) Tissue-type plasminogen activator deficiency exacerbates arthritis. J Immunol 167(2):1047-52 |
| abstractText | Fibrin deposition, cell migration, and tissue remodeling are key components in the lesions of inflammatory joint diseases, such as rheumatoid arthritis. The plasminogen activators (PAs), namely, tissue-type PA (t-PA) and urokinase PA, are implicated in these aspects of an inflammatory response, although their precise roles are yet to be defined. We therefore used gene-deficient mice to explore their role in a two-stage arthritis model involving intraarticular methylated BSA injection, followed by systemic IL-1 treatment. We report in this study that both t-PA and urokinase PA are protective for the mild arthritis induced by intraarticular methylated BSA injection alone, since absence of either of them exacerbates the response; following s.c. IL-1 injection, t-PA(-/-) mice had particularly severe disease. Fibrin deposition appeared to parallel disease severity under the various conditions, suggesting that PA-mediated fibrinolysis may be normally playing a protective role in inflammatory joint disease. |
