Myelin specific cells infiltrate MCAO lesions and exacerbate stroke severity

Xuefang Ren, Kozaburo Akiyoshi, Marjorie Grafe, Arthur Vandenbark, Patricia D. Hurn, Paco S. Herson, Halina Offner

Research output: Contribution to journalArticle

34 Scopus citations

Abstract

Although inflammatory responses increase stroke severity, the role of immune cells specific for central nervous system (CNS) antigens remains controversial. Disruption of the blood-brain barrier (BBB) during stroke allows CNS antigens to leak into the peripheral circulation and enhances access of circulating leukocytes to the brain, including those specific for CNS antigens such as myelin oligodendrocyte glycoprotein (MOG) that can induce experimental autoimmune encephalomyelitis (EAE). We here demonstrate for the first time that myelin reactive splenocytes specific for MOG transferred into severe combined immunodeficient (SCID) mice can migrate into the infarct hemisphere of recipients subjected to 60 min middle cerebral artery occlusion (MCAO) and 96 h reperfusion; moreover these cells exacerbate infarct volume and worsen neurological deficits compared to animals transferred with naïve splenocytes. These findings indicate that autoimmunity in the CNS can exert detrimental injury on brain cells and worsen the damage from ischemic stroke.

Original languageEnglish (US)
Pages (from-to)7-15
Number of pages9
JournalMetabolic Brain Disease
Volume27
Issue number1
DOIs
Publication statusPublished - Mar 2012

    Fingerprint

Keywords

  • Experimental stroke
  • Inflammatory responses
  • Myelin reactive splenocytes
  • Neurologic deficit

ASJC Scopus subject areas

  • Clinical Neurology
  • Biochemistry
  • Cellular and Molecular Neuroscience

Cite this