T-cell interleukin-6 receptor binding in interferon-beta-1b-treated multiple sclerosis patients

Multiple sclerosis (MS) is a T-cell-mediated autoimmune demyelinating disea se of the central nervous system, associated with an altered cytokine netwo rk. We previously assayed peripheral blood T-lymphocyte binding for two pro totypic cytokines, tumour necrosis factor-alpha (TNF-alpha) and interleukin -6 (IL-6), and found that T cells from MS patients had significantly more T NF-alpha and IL-6 receptors than those from healthy controls. In the presen t work, paralleling a previous one on T-cell TNF-alpha binding, we studied the effect of interferon (IFN)-beta -1b treatment on T-lymphocyte IL-6 bind ing in patients with relapsing-remitting MS. T cells from MS patients had s ignificantly (P < 0.001) higher amounts of IL-6 receptors than those from c ontrols [292 +/- 6 vs. 228 +/- 8 (mean +/- SEM) receptors per cell, respect ively], whereas the ligand-receptor affinity values were similar in the two groups [26.2 +/- 0.7 and 25.7 +/- 0.4 (mean +/- SEM) pmoles/1, respectivel y]. After a 3-month IFN-<beta>-1b treatment, they showed a significant decr ease in IL-6 binding [266 +/- 7 (mean +/- SEM) receptors per cell]. After 6 and 9 months, T-cell IL-6 B-max values were even lower [258 +/- 8 and 251 +/- 8 (mean +/- SEM) receptors per cell]. Since an increased IL-6 binding m ight be linked to a lymphocyte activation, our data give further support fo r an enhanced immune response in patients with MS. Our data seem to demonst rate that the major effects of IFN-beta -1b treatment result in a decrease of T-cell activation.