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.

Department of Microbiology and Immunology Cornell Center for Immunology Cornell Institute for Host Microbe Interactions and Disease Cornell Center for Health Equity Cornell University Ithaca NY USA

Institute for Clinical Chemistry and Laboratory Medicine University Clinic Technische Universität Dresden Dresden Germany

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

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