T cells are implicated in the pathogenesis of many inflammatory diseases. To fully activate T cells, both TCR and costimulatory molecule delivered signals are required (Lanzavecchia and Sallusto, 2000). Costimulation blockade targeting various costimulatory molecules seems to be an attractive therapeutic approach for the treatment of T cell-dependent autoimmune diseases. However, these strategies appear to be prophylactic rather than therapeutic, since naive T cell activation are more dependent on costimulatory signaling while the function of preexisting autoreactive T cells are less costimulation-dependent. Another shortcoming of this approach is its requirement of repeated long-lasting treatments, which is costly. Promisingly, recent studies showed that costimulatory agonists of CD137 could prevent and have therapeutic effects on CD4+ T cell-mediated organ-specific autoimmune disease such as experimental autoimmune encephalomyelitis (EAE) and experimental autoimmune uveitis (EAU) (Shao et al., 2005; Sun et al., 2002b), and both CD4+ T cell and autoantibody-involved systemic autoimmune diseases such as systemic lupus erythematosus (SLE), collagen type II-induced arthritis (CIA) and chronic graft-versus-host disease (cGVHD) (Foell et al., 2003, 2004; Kim et al., 2005; Seo et al., 2004; Sun et al., 2002a).
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