J Neuroimmunol. 2013 Jan 15;254(1-2):76-82. doi: 10.1016/j.jneuroim.2012.09.010. Epub 2012 Sep 29. Asgari N, Khorooshi R, Lillevang ST, Owens T. Source Neurobiology, Institute of Molecular Medicine,…
Asgari N, Khorooshi R, Lillevang ST, Owens T. Source Neurobiology, Institute of Molecular Medicine, University of Southern Denmark, J.B. Winsloewsvej 25, DK-5000 Odense C, Denmark;…
Abstract Objective.
Multiple sclerosis: pathology and pathogenesis Monday, May 30, 2011, 17:15 – 18:15 The pathology of fulminant neuromyelitis optica with extremely high level of serum anti aquaporin 4 antibody K. Maruyama, M.
How high doses of intravenous IgG (IVIG) suppress autoimmune diseases remains unresolved. We have recently shown that the antiinflammatory activity of IVIG can be attributed to a minor species of IgGs that is modified with terminal sialic acids on their Fc-linked glycans.
There is a complex, diverse array of “preceding environmental events” and perhaps unconnected immune-related events which are often associated with the period before patients are diagnosed with NMO. In this review we discuss in detail how the different isoform structures of AQP4 in different membrane locales and in different cell types might be related to pathology. Changes in AQP4 expression in CNS and non-CNS tissue can be regulated by inflammatory mediators induced during and following infection or by underlying autoimmunity and can result in the induction of AQP4-specific lymphocytes and ensuing pathogenesis.