IL-9 signaling affects central nervous system resident cells during inflammatory stimuli.
Publication/Presentation Date
12-1-2015
Abstract
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.
Volume
99
Issue
3
First Page
570
Last Page
574
ISSN
1096-0945
Published In/Presented At
Ding, X., Cao, F., Cui, L., Ciric, B., Zhang, G. X., & Rostami, A. (2015). IL-9 signaling affects central nervous system resident cells during inflammatory stimuli. Experimental and molecular pathology, 99(3), 570–574. https://doi.org/10.1016/j.yexmp.2015.07.010
Disciplines
Business Administration, Management, and Operations | Health and Medical Administration | Management Sciences and Quantitative Methods
PubMedID
26216406
Department(s)
Administration and Leadership
Document Type
Article