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

Paula Sanchis, Olaya Fernández-Gayol, Gemma Comes, Anna Escrig, Mercedes Giralt, Richard D. Palmiter, Juan Hidalgo Pareja*

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

5 Citations (Scopus)

Abstract

Background: 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. Methods: 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 (MOG35-55) peptide dissolved in complete Freund’s adjuvant (CFA) and supplemented with Mycobacterium tuberculosis. Results and conclusions: 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.
Original languageEnglish
Article number330
Pages (from-to)330
Number of pages18
JournalCells
Volume9
Issue number2
DOIs
Publication statusPublished - Feb 2020

Keywords

  • ASTROCYTES
  • IL-6
  • IL-6-DEFICIENT MICE
  • IN-VIVO
  • INDUCTION
  • MICROGLIA
  • MOG(35-55)peptide
  • MULTIPLE-SCLEROSIS
  • NF-KAPPA-B
  • T-CELLS
  • TH17 CELLS
  • conditional IL-6 knockout
  • experimental autoimmune encephalomyelitis
  • neuroinflammation

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