IL-9 signaling affects central nervous system resident cells during inflammatory stimuli

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• 作者：Xiaoli Ding^a ; ^b ; ¹ ; Fang Cao^c ; ¹ ; Langjun Cui^b ; Bogoljub Ciric^a ; Guang-Xian Zhang^a ; Abdolmohamad Rostami^a ; ^{a.m.rostami@jefferson.edu" class="auth_mail" title="E-mail the corresponding author}
• 关键词：IL-9 ; IL-9 receptor ; CNS resident cells ; Experimental autoimmune encephalomyelitis
• 刊名：Experimental and Molecular Pathology
• 出版年：2015
• 出版时间：December 2015
• 年：2015
• 卷：99
• 期：3
• 页码：570-574
• 全文大小：876 K

文摘

Interleukin (IL) 9, a dominant cytokine in Th9 cells, has been proven to play a pathogenic role in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), by augmenting T cell activation and differentiation; however, whether IL-9 signaling affects central nervous system (CNS)-resident cells during CNS autoimmunity remains unknown. In the present study, we found that the IL-9 receptor (IL-9R) was highly expressed in astrocytes, oligodendrocyte progenitor cells (OPCs), oligodendrocytes and microglia cells, and that its expression was significantly upregulated in brain and spinal cord during EAE. In addition, IL-9 increased chemokine expression, including CXCL9, CCL20 and MMP3, in primary astrocytes. Although IL-9 had no effect on the proliferation of microglia cells, it decreased OPC proliferation and differentiation when in combination with other pro-inflammatory cytokines, but not with IFN-γ. IL-9 plus IFN-γ promoted OPC proliferation and differentiation. These findings indicate that CNS-restricted IL-9 signaling may be involved in the pathogenesis of MS/EAE, thus providing a potential therapeutic target for future MS/EAE treatment through disruption of CNS cell-specific IL-9 signaling.