Background and objectives
Activated T cells play a central role in the inflammatory cascade leading to the joint inflammation and destruction characteristic of rheumatoid arthritis (RA). The cytokines secreted by activated T cells are thought to both initiate and propagate the immunologically driven inflammation associated with RA.
Abatacept, the first of a new class of agents for the treatment of RA that selectively modulates the co-stimulatory signal required for full T-cell activation, was evaluated for its ability to regulate human T-cell proliferation and cytokine production in vitro. The effect of abatacept on lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNF-α) from monocytes was evaluated to distinguish the impact of this agent on innate versus adaptive, antigen-specific immune responses.