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

• Enhanced eosinophil numbers in the spinal cord in the course of EAE. • Absence of eosinophils has no impact on clinical development or severity of EAE. • Spinal cord inflammation and demyelination is not affected by eosinophil deficiency. 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 MOG 35–55 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. [ABSTRACT FROM AUTHOR]