Does inflammation stimulate remyelination?

Abstract

■ Abstract The traditional view of the disease process in multiple sclerosis considered inflammation in the central nervous system as solely detrimental, with demyelination as the key consequence. However, recent evidence suggests that inflammation also can be beneficial and even have neuroprotective effects due to 'cross-talk' between the nervous and immune systems. Immune cells release a number of neurotrophic factors upon activation, including BDNF, neurotrophin-3, leukaemia inhibitory factor (LIF), and neurturin. Secretion of these factors within the nervous system during an active inflammatory episode in multiple sclerosis might protect neurones from injury. Glatiramer acetate can stimulate the release of BDNF from reactive Th2 cells, and this may contribute to a neuroprotective effect of this treatment. In addition, factors released from immune cells may have positive effects on remyelination, eliciting migration and differentiation of oligodendrocyte precursor cells and promoting survival of mature oligodendrocytes. Harnessing the beneficial effects of inflammation represents a promising therapeutic approach to improving treatment of multiple sclerosis.