RNA-seq of TCR-stimulated CD4? T cells from SKG mice treated with the Nr4a1 agonist Cytosporone B

Rheumatoid arthritis (RA) is a chronic autoimmune disease in which CD4? T cells and T helper 17 (Th17) cells play central roles in driving synovial inflammation. Nr4a1 is an orphan nuclear receptor that acts as a negative regulator of T cell activation. Cytosporone B (CsnB) is a small-molecule Nr4a1 agonist with immunomodulatory properties, but its impact on T cell responses in autoimmune arthritis remains unclear. In this study, we used SKG mice, a T cell–driven model of chronic autoimmune arthritis, to investigate how pharmacologic Nr4a1 activation influences pathogenic T cell responses. CD4? T cells isolated from SKG mice were stimulated through the T cell receptor in vitro in the presence or absence of CsnB, and transcriptomic profiling was performed by RNA sequencing. The resulting dataset provides genome-wide information on CsnB-induced changes in gene expression in activated CD4? T cells, and supports mechanistic analyses of how Nr4a1 activation modulates T cell activation and Th17-related pathways in autoimmune arthritis. Overall design: Total CD4? T cells were isolated from spleens and lymph nodes of SKG mice using magnetic-activated cell sorting. Purified CD4? T cells were stimulated in vitro on plates coated with anti-CD3 and anti-CD28 antibodies in the presence or absence of the Nr4a1 agonist Cytosporone B (CsnB) for 2 hours.