CD4 and rheumatoid arthritis: For instance, patients with systemic lupus erythematosus (SLE) demonstrate an increase in T helper 1 (Th1) relative to T helper 2 (Th2) cells and a dysregulated balance between Th1 and T helper 17 (Th17) cells, while results from single cell sequencing of patients with rheumatoid arthritis (RA) have demonstrated a skewing toward Th1 effector memory CD4+ T cells, and a murine model of multiple sclerosis (MS) showed resistance to disease development due, in part, to a loss of key T cell intrinsic Th1 mediators (1–4).