中枢神经系统固有细胞对淋巴细胞的抗原提呈作用的研究

he pathogenic mechanisms of multiple sclerosis (MS) is still unclear. Presently, MS is considered as autoimmune disease caused by central nervous system(CNS) infections. There is interaction between resident cells of the CNS and infiltrating lymphocytes. During the development of experimental autoimmune encephalitomyelitis (EAE), the astrocytes，which is considered as the resident cells of the central nervous system, could inhibit MOG35-55-specific lymphocytes. However, when astrocytes were pretreated with IFN-γ, they could promote the proliferation and secretion levels of MOG35-55-specific lymphocytes, coinciding with apparent expression of major histocompatibility complex (MHC)-II on astrocytes themselves. Quantitative polymerase chain reaction (qPCR) demonstrated that production of IFN-γ in the spinal cord was highest during the peak phase. Quantitative analysis of MHC-II expression in the spinal cord showed that there was a positive correlation between MHC-II expression and IFN-γ production. In addition, astrocyte MHC-II expression levels correlated positively with IFN-γ production in the spinal cord. These findings suggested that astrocytes might function as promoters of EAE. Then, in the presence of higher IFN-γ levels in the spinal cord, astrocytes were converted into antigen-presenting cells. This conversion might promote the progression of pathological damage and result in a peak of EAE severity.