CORD-19:16a812de72963ceda960a168236e8dbe91832d45 / 40080-40929 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/CORD-19/sourceid/16a812de72963ceda960a168236e8dbe91832d45","sourcedb":"CORD-19","sourceid":"16a812de72963ceda960a168236e8dbe91832d45","text":"When antibodies to myelin oligodendrocyte glycoprotein (MOG) are injected after the induction of EAE, the severity of the disease is dramatically increased and large demyelinating lesions develop (Genain et al., 1995; Linington et al., 1992; Schluesener et al., 1987) . In addition, antibodies to MOG have been detected in association with disintegrating myelin in both human MS patients and in a marmoset model of EAE (Genain et al., 1999) . Likewise, EAE-like Type II MS lesions, responsible for 30% to 50% of lesions in patients, are characterized by the deposition of immunoglobulin and complement (Lucchinetti et al., 1998 . Finally, we have shown that plasma exchange is effective in approximately 40% of cases with fulminant MS exacerbations, suggesting the presence of pathogenic autoantibodies in these patients (Weinshenker et al., 1999) 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