1. Academic Validation
  2. Eosinophils are dispensable for development of MOG35-55-induced experimental autoimmune encephalomyelitis in mice

Eosinophils are dispensable for development of MOG35-55-induced experimental autoimmune encephalomyelitis in mice

  • Immunol Lett. 2021 Nov;239:72-76. doi: 10.1016/j.imlet.2021.09.001.
Klara Ruppova 1 Jong-Hyung Lim 1 Georgia Fodelianaki 1 Avery August 2 Ales Neuwirth 3
Affiliations

Affiliations

  • 1 Institute for Clinical Chemistry and Laboratory Medicine, University Clinic, Technische Universität Dresden, Dresden, Germany.
  • 2 Department of Microbiology & Immunology, Cornell Center for Immunology, Cornell Institute for Host-Microbe Interactions & Disease, Cornell Center for Health Equity, Cornell University, Ithaca, NY, USA.
  • 3 Institute for Clinical Chemistry and Laboratory Medicine, University Clinic, Technische Universität Dresden, Dresden, Germany; Laboratory of Adaptive Immunity, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czech Republic. Electronic address: [email protected].
Abstract

Experimental autoimmune encephalomyelitis (EAE) represents the mouse model of multiple sclerosis, a devastating neurological disorder. EAE development and progression involves the infiltration of different immune cells into the brain and spinal cord. However, less is known about a potential role of eosinophil granulocytes for EAE disease pathogenesis. In the present study, we found enhanced eosinophil abundance accompanied by increased concentration of the eosinophil chemoattractant eotaxin-1 in the spinal cord in the course of EAE induced in C57BL/6 mice by immunization with MOG35-55 peptide. However, the absence of eosinophils did not affect neuroinflammation, demyelination and clinical development or severity of EAE, as assessed in ∆dblGATA1 eosinophil-deficient mice. Taken together, despite their enhanced abundance in the inflamed spinal cord during disease progression, eosinophils were dispensable for EAE development.

Keywords

Autoimmunity; Demyelination; EAE; Eosinophils; MOG.

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