Background and objectives
Rheumatoid arthritis is an autoreactive disease in which activated T cells play an important role orchestrating the autoimmune responses giving rise to the inflammatory cascade responsible for joint inflammation and bone destruction. The CD28/B7 costimulatory pathway is critical for full T-cell activation, and modulating this pathway has been shown to inhibit T-cell activation leading to inhibition of these immune responses. Abatacept modulates T-cell activation by interfering with the engagement of CD80/86 with CD28. Abatacept has been shown to provide significant improvement in the signs and symptoms of rheumatoid arthritis in a phase II trial. Here, we examine the effect abatacept administration has on disease induction, anti-collagen antibody production and bone destruction in a rat model of collagen-induced arthritis.