CNS Remyelination and the Innate Immune System.
CNS Remyelination and the Innate Immune System.
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DOI：
10.3389/fcell.2016.00038
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发表时间：
2016
影响因子：
5.5
通讯作者：
Franklin RJ
中科院分区：
文献类型：
--
作者：
McMurran CE;Jones CA;Fitzgerald DC;Franklin RJ
误导性炎症反应常与髓鞘损伤有关。多发性硬化症(MS)是一种自身免疫性疾病，其病因以免疫介导的损伤为中心，在髓鞘疾病中尤为突出。然而，强烈的炎症反应对于这种损伤后髓鞘的有效再生也是必不可少的。在这里，我们讨论促进再髓鞘形成的炎症功能，以及这些功能是如何通过实验从免疫反应的病理方面分离出来的。我们专注于常驻小胶质细胞和单核细胞来源的巨噬细胞对重新髓鞘形成的贡献，并比较这两类天然免疫细胞的作用。最后，目前的文献是在开发治疗的背景下，操纵先天免疫反应，以促进临床髓鞘疾病的重新髓鞘形成。
A misguided inflammatory response is frequently implicated in myelin damage. Particularly prominent among myelin diseases, multiple sclerosis (MS) is an autoimmune condition, with immune–mediated damage central to its etiology. Nevertheless, a robust inflammatory response is also essential for the efficient regeneration of myelin sheaths after such injury. Here, we discuss the functions of inflammation that promote remyelination, and how these have been experimentally disentangled from the pathological facets of the immune response. We focus on the contributions that resident microglia and monocyte-derived macrophages make to remyelination and compare the roles of these two populations of innate immune cells. Finally, the current literature is framed in the context of developing therapies that manipulate the innate immune response to promote remyelination in clinical myelin disease.