(a) Effector Tregs (eTregs) most strongly affect CD8-EM cells and B-plasma cells. (b) A closer look reveals eTregs control CD8-EM cells by stopping their division and reducing GzmB while maintaining CD27. (c) Dividing eTregs increase CD98, GLUT1, and CTLA4 proteins, and shows how an anti-CTLA4 antibody affects this process. (d) Reveals a potential biomarker by showing two distinct types of eTregs: one expressing HLA-DR and CCR4, and another expressing CD38 and CCR7 - a pattern seen in severe viral infections. (e) Ranks different Treg types by their suppressive ability, with eTregs being strongest. (f) Demonstrates how the drug Tazemetostat blocks naive Tregs from becoming eTregs during early cell division.