Endogenously regulated Dab2 worsens inflammatory injury in experimental autoimmune encephalomyelitis.

ABSTRACT:

Background

Neuroinflammation regulates both disease pathogenesis and repair in multiple sclerosis. In early multiple sclerosis lesion development, neuroinflammation causes demyelination and axonal injury, the likely final common determinant of disability. Here we report the identification of a novel neuroinflammatory mediator, Disabled-2 (Dab2). Dab2 is an intracellular adaptor protein with previously unknown function in the central nervous system.

Results

We report that Dab2 is up-regulated in lesional macrophages/microglia in the spinal cord in murine experimental autoimmune encephalomyelitis, a model of multiple sclerosis. We demonstrate that dab2 expression is positively correlated with experimental autoimmune encephalomyelitis disease severity during the acute disease p

SUBMITTER: Jokubaitis VG 

PROVIDER: S-EPMC3893401 | biostudies-literature | 2013 Jul

REPOSITORIES: biostudies-literature