星形胶质细胞在实验性自身免疫性脑脊髓炎发病早期对浸润淋巴细胞的影响

he nature of pathogenic mechanisms associated with the development of multiple sclerosis (MS) have long been debated. However, limited research was conducted to define the interplay between infiltrating lymphocytes and resident cells of the central nervous system (CNS). Data presented in this report describe a novel role for astrocyte-mediated alterations to myelin oligodendrocyte glycoprotein (MOG)35-55-specific lymphocyte responses, elicited during the development of experimental autoimmune encephalitomyelitis (EAE). In-vitro studies demonstrated that astrocytes inhibited the proliferation and interferon (IFN)-γ, interleukin (IL)-4, IL-17 and transforming growth factor (TGF)-β secretion levels of MOG35-55-specific lymphocytes, an effect that could be ameliorated by astrocyte IL-27 neutralization. Quantitative polymerase chain reaction (qPCR) demonstrated that production of IL-27 in the spinal cord was at its highest during the initial phases. These findings suggested that astrocytes might function as inhibitors of EAE. Astrocytes prevented MOG35-55-specific lymphocyte function by secreting IL-27 during the initial phases of EAE.