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The Journal of Immunology, 2001, 167: 1047-1052.
Copyright © 2001 by The American Association of Immunologists

Tissue-Type Plasminogen Activator Deficiency Exacerbates Arthritis1

Yuan H. Yang2,*, Peter Carmeliet{dagger} and John A. Hamilton*

* Department of Medicine, Arthritis and Inflammation Research Centre, University of Melbourne, Royal Melbourne Hospital, Parkville, Victoria, Australia; and {dagger} Centre for Transgenic Technology and Gene Therapy, Flanders Interuniversity, Leuven, Belgium

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.




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