Which agent for RA prevents full T-cell activation by competing with CD28?

The correct answer is the agent that prevents full T-cell activation by competing with CD28, which is crucial in the activation process of T-cells. Abatacept is a fusion protein that consists of the extracellular domain of CTLA-4 fused to IgG1. Its mechanism of action involves binding to CD80 and CD86 on antigen-presenting cells, thereby blocking the interaction with CD28 on T-cells. This competition prevents the necessary co-stimulatory signal that T-cells require for full activation. Without this signal, T-cell activation is inhibited, leading to decreased inflammation and joint damage associated with rheumatoid arthritis (RA).

Other agents mentioned, such as Sarilumab, Golimumab, and Adalimumab, work via different mechanisms. For instance, Sarilumab is an interleukin-6 receptor antagonist; Golimumab and Adalimumab are both tumor necrosis factor (TNF) inhibitors. While they are effective in treating RA, they do not interfere with the CD28 pathway specifically. Thus, Abatacept is uniquely positioned in clinical pharmacology for its ability to disrupt T-cell activation by competing with CD28, making it the correct choice for this question.