Multiple sclerosis (MS) is a T-cell-mediated autoimmune demyelinating disease of the central nervous system, associated with an altered cytokine network. We previously assayed peripheral blood T-lymphocyte binding for two prototypic cytokines, tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6), and found that T cells from MS patients had significantly more TNF-α and IL-6 receptors than those from healthy controls. In the present work, paralleling a previous one on T-cell TNF-α binding, we studied the effect of interferon (IFN)-β-1b treatment on T-lymphocyte IL-6 binding in patients with relapsing–remitting MS. T cells from MS patients had significantly (P < 0.001) higher amounts of IL-6 receptors than those from controls [292 ± 6 vs. 228 ± 8 (mean ± SEM) receptors per cell, respectively], whereas the ligand-receptor affinity values were similar in the two groups [26.2 ± 0.7 and 25.7 ± 0.4 (mean ± SEM) pmoles/l, respectively]. After a 3-month IFN-β-1b treatment, they showed a significant decrease in IL-6 binding [266 ± 7 (mean ± SEM) receptors per cell]. After 6 and 9 months, T-cell IL-6 Bmax values were even lower [258 ± 8 and 251 ± 8 (mean ± SEM) receptors per cell]. Since an increased IL-6 binding might be linked to a lymphocyte activation, our data give further support for an enhanced immune response in patients with MS. Our data seem to demonstrate that the major effects of IFN-β-1b treatment result in a decrease of T-cell activation.