Hematogenous macrophages and resident brain microglia are agents of de
myelination in multiple sclerosis (MS) and paradoxically may also part
icipate in remyelination. In vitro studies have shown that macrophage
enrichment of aggregate brain cultures promotes myelination per se and
enhances the capacity to remyelinate following a demyelinating episod
e. It has been hypothesized that remyelination in MS is implemented by
surviving dedifferentiated oligodendrocytes or by newly recruited pro
genitors that migrate, proliferate and synthesize myelin in response t
o signalling molecules in the local environment. We postulate that mac
rophage-derived cytokines or growth factors may directly or indirectly
promote oligodendroglial proliferation and differentiation, contribut
ing to myelin repair in inflammatory demyelinating disease.