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.