Protective effect of an elastase inhibitor in a neuromyelitis optica-like disease driven by a peptide of myelin oligodendroglial glycoprotein.

ABSTRACT:

Background

The pathology of neuromyelitis optica (NMO), in contrast to multiple sclerosis, comprises granulocyte infiltrates along extensive lengths of spinal cord, as well as optic nerve. Furthermore, IFN-β treatment worsens NMO. We recently found that experimental autoimmune encephalomyelitis (EAE) induced with Th17 cells is exacerbated by IFN-β, in contrast to disease induced with Th1 where treatment attenuated symptoms.

Objective

This study demonstrates the similarities between NMO and Th17 EAE and how neutrophils mediate pathology in Th17 disease.

Methods

Levels of blood biomarkers in NMO were assessed by Luminex and ELISA. Effects of IFN-β on neutrophils were assessed by culture assays and immunofluorescence. EAE was induced by transfer of myelin-specific Th1 or

SUBMITTER: Herges K 

PROVIDER: S-EPMC3319834 | biostudies-literature | 2012 Apr

REPOSITORIES: biostudies-literature