Interleukin-6 Derived from the Central Nervous System May Influence the Pathogenesis of Experimental Autoimmune Encephalomyelitis in a Cell-Dependent Manner

Interleukin-6 (IL-6) is a pleiotropic and multifunctional cytokine that plays a critical role in induction of experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS). Although EAE has always been considered a peripherally elicited disease, Il6 expression exclusively...

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Bibliographic Details
Published in:Cells (Basel, Switzerland) Switzerland), 2020-01, Vol.9 (2), p.330
Main Authors: Sanchis, Paula, Fernández-Gayol, Olaya, Comes, Gemma, Escrig, Anna, Giralt, Mercedes, Palmiter, Richard D, Hidalgo, Juan
Format: Article
Language:English
Subjects:
Animals
Central Nervous System - metabolism
conditional il-6 knockout
CX3C Chemokine Receptor 1 - metabolism
Demyelinating Diseases - pathology
Encephalomyelitis, Autoimmune, Experimental - genetics
Encephalomyelitis, Autoimmune, Experimental - pathology
experimental autoimmune encephalomyelitis
Female
Gene Expression Regulation
Glial Fibrillary Acidic Protein - metabolism
Gliosis - pathology
Inflammation - genetics
Inflammation - pathology
Interleukin-6 - metabolism
Male
Mice, Inbred C57BL
Mice, Knockout
mog35-55peptide
Myelin-Oligodendrocyte Glycoprotein - metabolism
neuroinflammation
Spinal Cord - pathology
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Summary:Interleukin-6 (IL-6) is a pleiotropic and multifunctional cytokine that plays a critical role in induction of experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS). Although EAE has always been considered a peripherally elicited disease, Il6 expression exclusively within central nervous system is sufficient to induce EAE development. Neurons, astrocytes, and microglia can secrete and respond to IL-6. To dissect the relevance of each cell source for establishing EAE, we generated and immunized conditional Il6 knockout mice for each of these cell types with myelin oligodendrocyte glycoprotein 35-55 (MOG ) peptide dissolved in complete Freund's adjuvant (CFA) and supplemented with Mycobacterium tuberculosis. The combined results reveal a minor role for Il6 expression in both astrocytes and microglia for symptomatology and neuropathology of EAE, whereas neuronal Il6 expression was not relevant for the variables analyzed.
ISSN:2073-4409
2073-4409
DOI:10.3390/cells9020330