A prospective study of the expression of the chemokine receptor CCR7 was performed in 11 relapsing-remitting multiple sclerosis (MS) patients during 12 months of interferon-beta (IFNbeta) treatment. The results show increased expression of CCR7 on peripheral blood lymphocytes (PBL) of MS patients receiving IFNbeta treatment as well as lymphocytes from healthy subjects treated with IFNbeta in vitro. Our results suggest that in addition to modulating the expression of adhesion molecules, the mode of action of IFNbeta also involves the control of the chemokine receptor CCR7. The net effect is a key change in the control of lymphocyte traffic between immune organs and the central nervous system (CNS) and a shift from CCR7 negative effector T cells to CCR7 positive central memory T cells.