There is no doubt about the immunomodulatory capacity of intravenous immunoglobulins (IVIg). This also holds true for multiple sclerosis (MS), where clinical trials have shown a reduction in relapse rate and number of active lesions on MRI after IVIg treatment. Experimental data in the model of murine Theiler's virus encephalomyelitis (TMEV) gave rise to the hypothesis that IVIg may also promote remyelination. Unfortunately, recent trials were unable to demonstrate clinically relevant remyelination in MS patients treated with IVIg. A possible explanation could lie in the fact that IVIg do not influence the function of oligodendrogilial cells in vitro. In contrast, IVIg can protect oligodendrocytes against complement-mediated injury and thus provide more cells that could engage in remyelination. In addition, IVIg can modulate microglial functions in vitro, thus creating a microenvironment permissive for remyelination. Should such mechanisms also be operative in vivo, they would have escaped detection in the treatment protocols used to date. It would appear that IVIg need to be administered while the inflammatory process is still ongoing, whereas the published trials included only patients with a stable deficit when there is probably little or no active inflammation. Despite new studies on IVIg, its role in the management of MS remains elusive.