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Journal of Biomedicine and Biotechnology
Volume 2010 (2010), Article ID 357412, 12 pages
Review Article

The Role of Apolipoprotein E in Guillain-Barré Syndrome and Experimental Autoimmune Neuritis

1Department of Neurology, The First Hospital of Jilin University, 130021, Changchun, China
2Department of Neurobiology, Care Sciences and Society, Karolinska Institute, Karolinska University Hospital Huddinge, SE-141 86, Stockholm, Sweden

Received 12 October 2009; Accepted 20 December 2009

Academic Editor: Don Mark Estes

Copyright © 2010 Hong-liang Zhang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Apolipoprotein E (apoE) is a 34.2 kDa glycosylated protein characterized by its wide tissue distribution and multiple functions. ApoE has been widely studied in lipid metabolism, cardiocerebrovascular diseases, and neurodegenerative diseases like Alzheimer's disease and mild cognitive impairment, and so forth. Recently, a growing body of evidence has pointed to nonlipid related properties of apoE, including suppression of T cell proliferation, regulation of macrophage function, facilitation of lipid antigen presentation by CD1 molecules to natural killer T (NKT) cells, and modulation of inflammation and oxidation. By these properties, apoE impacts physiology and pathophysiology at multiple levels. The present paper summarizes updated studies on the immunoregulatory function of apoE, with special focus on isoform-specific effects of apoE on Guillain-Barré syndrome (GBS) and its animal model experimental autoimmune neuritis (EAN).