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J Neuroimmunol. 2015 Jan 15;278:112-22. doi: 10.1016/j.jneuroim.2014.12.009. Epub 2014 Dec 11.

Dynamic changes in meningeal inflammation correspond to clinical exacerbations in a murine model of relapsing-remitting multiple sclerosis.

Author information

1
Department of Microbiology and Immunology, Northwestern University Feinberg School of Medicine, Chicago, IL, United States.
2
Department of Microbiology and Immunology, Northwestern University Feinberg School of Medicine, Chicago, IL, United States. Electronic address: m-brown12@northwestern.edu.

Abstract

Inflammation in the meninges, tissues surrounding the brain and spinal cord that enclose the cerebrospinal fluid, closely parallels clinical exacerbations in relapsing-remitting experimental autoimmune encephalomyelitis (EAE). In preclinical disease, an influx of innate immune cells precedes loss of blood brain barrier (BBB) integrity and large-scale inflammation in the central nervous system (CNS). T cell infiltration into the meninges is observed in acute disease as well as during relapse, when neither BBB permeability nor significant increases in peripherally-derived immune cell numbers in the CNS are observed. These findings support the idea that the meninges are a gateway for immune cell access into the CNS, a finding that has important therapeutic implications.

KEYWORDS:

Blood brain barrier (BBB); CNS demyelinating disease; Experimental autoimmune encephalomyelitis (EAE); Meninges; Multiple sclerosis (MS); Relapsing–remitting EAE

PMID:
25595260
DOI:
10.1016/j.jneuroim.2014.12.009
[Indexed for MEDLINE]

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