Non-lytic autoantibody mediated effects on myelination are associated with increased pro-inflammatory chemokine expression

Abstract

Multiple sclerosis is associated with intrathecal synthesis of immunoglobulins directed against sulphatide, a major CNS myelin glycolipid. To explore the clinical/pathological relevance of this response we investigated the effect of treating myelinating cultures with a sulphatide-reactive IgM mouse monoclonal antibody (O4). In the absence of an exogenous source of complement the mAb was unable to induce demyelination, but inhibited myelination, an effect associated with microglial proliferation and activation.