Modulating the co-stimulatory signal for T cell activation in rheumatoid arthritis: Could it be the first step of the treatment?

• Abatacept inhibits the co-stimulation of T cells and disrupts the pathways that lead to joint inflammation and structural damage.
• Abatacept represents an effective treatment option in RA with inadequate response to non-biological DMARDs
• In early RA abatacept significantly impacts disease activity and structural damage

Advances in our understanding of the key mediators of chronic inflammation and tissue damage in rheumatoid arthritis (RA) have fostered the development of targeted therapies and greatly expanded the available treatment options. Abatacept, a soluble human fusion protein that selectively modulates the co-stimulatory signal required for full T-cell activation, is approved for the treatment of moderate to severe RA in the United States, Canada, and the European Union. This review summarises the data on efficacy (disease activity, quality of life, prevention of structural damage) and safety from randomised clinical trials of abatacept plus methotrexate in patients with: i) active RA and an inadequate response to methotrexate who are naïve to biological disease-modifying anti-rheumatic drugs; and ii) methotrexate-naïve early RA with poor prognostic factors. Novel imaging outcomes and biological changes induced by abatacept treatment are also briefly reviewed. Optimal use of abatacept as a first-line biological therapy is discussed in light of the current recommendations and guidelines.