Oligodendrocytes and their progenitors are glial cells in the central nervous system, which have been mainly implicated with the homeostatic roles of axonal myelin ensheathment but serve as targets of the peripheral immune system attack in the context of diseases like multiple sclerosis. This view of oligodendroglia as passive bystanders with no immunological properties was first challenged in the 1980s when it was reported that the cytokine interferon γ could induce the gene expression of the major histocompatibility complexes (MHC) class I and II. While the physiological role of this induction was controversial for decades to follow, recent studies suggest that oligodendroglia survey their environment, respond to a larger array of cues and can indeed exert immunomodulatory functions, which are particularly relevant in the context of neurodegeneration and demyelinating diseases. The alternative functionality of oligodendroglia not only regulates immune cell responses, but also hinders remyelination, and might thereby be key to understanding MS disease pathology and promoting regeneration after immune-mediated demyelination.

少突胶质细胞及其祖细胞是中枢神经系统中的神经胶质细胞，主要与轴突髓鞘鞘的稳态作用有关，但在多发性硬化症等疾病的背景下可作为外周免疫系统攻击的目标。这种将少突胶质细胞视为没有免疫特性的被动旁观者的观点在 1980 年代首次受到挑战，当时有报道称细胞因子干扰素 γ 可以诱导 I 类和 II 类主要组织相容性复合物 (MHC) 的基因表达。虽然这种诱导的生理作用在接下来的几十年里一直存在争议，但最近的研究表明，少突胶质细胞会调查它们的环境，对更多的线索做出反应，并且确实可以发挥免疫调节功能，这在神经退行性疾病和脱髓鞘疾病的背景下特别相关。少突胶质细胞的替代功能不仅调节免疫细胞反应，而且阻碍髓鞘再生，因此可能是了解 MS 疾病病理学和促进免疫介导脱髓鞘后再生的关键。