Expression is enhanced by IL-2.
Function is controlled largely by regulation of its surface expression. Initially CTLA-4 is in the intracellular membrane but moves to the cell surface after T-cell receptor signaling.
When CTLA-4 cytoplasmic tail is NOT phosphorylated it binds to AP-2 (clathrin adapter molecule) and is removed from the surface. When the tail is phosphorylated AP-2 cannot bind and CTLA-4 is expressed on the surface.
CTLA-4 competes with CD28 for B7 ligand, and it has a higher affinity of B7 in part because CTLA-4 binds B7 in a dimer.
CTLA-4 interfers with the formation of lipid rafts, TCR:ZAP70 microclusters, and central supramolecular activation complex.