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Eosinophils are dispensable for development of MOG35-55-induced experimental autoimmune encephalomyelitis in mice
K. Ruppova, JH. Lim, G. Fodelianaki, A. August, A. Neuwirth
Jazyk angličtina Země Nizozemsko
Typ dokumentu časopisecké články
- MeSH
- chemokin CCL11 metabolismus MeSH
- encefalomyelitida autoimunitní experimentální krev diagnóza imunologie patologie MeSH
- eozinofily imunologie metabolismus MeSH
- glykoprotein v myelinu oligodendrocytů aplikace a dávkování imunologie MeSH
- lidé MeSH
- mícha imunologie patologie MeSH
- myši transgenní MeSH
- myši MeSH
- peptidové fragmenty aplikace a dávkování imunologie MeSH
- roztroušená skleróza krev diagnóza imunologie patologie MeSH
- stupeň závažnosti nemoci MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- myši MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
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.
Citace poskytuje Crossref.org
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- $a 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.
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