Diemel L T, Copelman C A, Cuzner M L
Miriam Marks Department of Neurochemistry, Institute of Neurology, London, UK. ldiemel@.ion.ucl.ac.uk
Neurochem Res. 1998 Mar;23(3):341-7. doi: 10.1023/a:1022405516630.
Hematogenous macrophages and resident brain microglia are agents of demyelination in multiple sclerosis (MS) and paradoxically may also participate 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 episode. It has been hypothesized that remyelination in MS is implemented by surviving dedifferentiated oligodendrocytes or by newly recruited progenitors that migrate, proliferate and synthesize myelin in response to signalling molecules in the local environment. We postulate that macrophage-derived cytokines or growth factors may directly or indirectly promote oligodendroglial proliferation and differentiation, contributing to myelin repair in inflammatory demyelinating disease.
血源性巨噬细胞和驻留脑小胶质细胞是多发性硬化症(MS)中脱髓鞘的介质,矛盾的是,它们也可能参与髓鞘再生。体外研究表明,聚集脑培养物中的巨噬细胞富集本身可促进髓鞘形成,并增强脱髓鞘发作后重新髓鞘化的能力。据推测,MS中的髓鞘再生是由存活的去分化少突胶质细胞或新招募的祖细胞实现的,这些祖细胞会迁移、增殖并响应局部环境中的信号分子合成髓磷脂。我们推测,巨噬细胞衍生的细胞因子或生长因子可能直接或间接促进少突胶质细胞的增殖和分化,有助于炎症性脱髓鞘疾病中的髓鞘修复。