Interferon-γ in Progression to Chronic Demyelination and Neurological Deficit Following Acute EAE ☆

摘要: The cytokine interferon-γ (IFNγ) is implicated in the induction of acute CNS inflammation, but it less clear what role if any IFNγ plays progression to chronic demyelination and neurological deficit. To address this issue, we have expressed myelinating oligodendrocytes transgenic mice. MHC I immunostaining iNOS mRNA were upregulated their CNS, such mice showed no spontaneous inflammation or demyelination, incidence, severity, histopathology experimental autoimmune encephalomyelitis (EAE) similar nontransgenic controls. In contrast control mice, which remit from EAE with resolution glial reactivity leukocytic infiltration, transgenics deficits. While activated microglia/macrophages persisted demyelinating lesions for over 100 days, CD4+T lymphocytes longer present CNS. therefore may play a long-term disability following disease. Because neural as well immune-infiltrating origins, these findings generate new perspective on its