To verify the hypothesis that blockade of CD28 costimulation by treatment with abatacept in patients with rheumatoid arthritis (RA) might induce a reduction in the number of CD28- T cells, as well as other effector T cell populations. We evaluated whether these variations correlate with clinical response.
Peripheral blood T cell subsets were longitudinally evaluated by flow cytometry through the analysis of CD28, CD45RA, and CCR7 expression in 16 patients with RA who were treated with abatacept.
After 48 weeks of treatment, the proportion and the absolute number of circulating CD8+CD28- T cells decreased (p = 0.008, p = 0.055, respectively, compared with baseline), as well as the proportion of the CD8+CD45RA+CCR7- cells, thought to represent terminally differentiated effector T cells (p = 0.03). Reductions of percentages of circulating CD4+CD28- and CD8+CD28- T cells, and (CCR7-) CD8+ total effector T cells were directly correlated with the reduction of Disease Activity Score 28 C-reactive protein (r = 0.58, p = 0.014; r = 0.47, p = 0.059; r = 0.59, p = 0.012, respectively).
After therapy with abatacept, circulating CD28- T cells and other effector populations decrease in patients with RA. This decrease is correlated with clinical response.