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Myelin specific cells infiltrate MCAO lesions and exacerbate stroke severity |
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| Authors: | Xuefang Ren Kozaburo Akiyoshi Marjorie R. Grafe Arthur A. Vandenbark Patricia D. Hurn Paco S. Herson Halina Offner |
| Affiliation: | (1) Department of Anesthesiology and Perioperative Medicine, Oregon Health & Science University, Portland, OR, USA;(2) Neuroimmunology Research, R&D31, Portland VA Medical Center, 3710 SW US Veterans Hospital Road, Portland, OR 97239, USA;(3) Department of Pathology, Oregon Health and Science University, Portland, OR, USA;(4) Department of Veterans Affairs Medical Center, Sr. Research Career Scientist, Research Service, Portland, OR, USA;(5) Department of Neurology, Oregon Health & Science University, Portland, OR, USA;(6) Department of Molecular Microbiology & Immunology, Oregon Health & Science University, Portland, OR, USA;(7) Office of Health Affairs, The University of Texas System, Austin, TX, USA;(8) Present address: Department of Anesthesiology and Critical Care Medicine, Kyushu University Hospital, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan; |
| 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 na?ve splenocytes. These findings indicate that autoimmunity in the CNS can exert detrimental injury on brain cells and worsen the damage from ischemic stroke. |
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