Butterfield RJ, Blankenhorn EP, Roper RJ, Zachary JF, Doerge RW, Sudweeks J, Rose J, Teuscher C
J Immunol 1999 Mar 1;162(5):3096-3102
Authors Addresses
PMID# 10072563
Abstract
Experimental Allergic EnCephaloMyelitis (EAE) is the principal animal model of Multiple Sclerosis (MS), the major Inflammatory Disease of the Central Nervous System. Murine EAE is generally either an Acute Monophasic or Relapsing disease.
Because the clinical spectrum of MS is more diverse, the limited range of Disease subtypes observed in EAE has raised concern regarding its relevance as a model for MS.
During the generation of a large F2 mapping population between the
EAE-susceptible SJL/J and EAE-resistant B10.S/DvTe inbred lines, we identified four distinct subtypes of Murine EAE resembling clinical subtypes seen in MS.
We observed Acute Progressive, Chronic/NonRemitting, Remitting/Relapsing, and Monophasic Remitting/NonRelapsing EAE.
An additional subtype, Benign EAE, was identified after Histologic examination revealed that some mice had Inflammatory infiltrates of the Central Nervous System, but did not show clinical signs of EAE.
Genome exclusion mapping was performed to identify the loci controlling susceptibility to each disease subtype. We report three novel EAE-modifying loci on Chromosomes 16, 7, and 13 (EAE11-13, respectively).
Additionally, unique loci with Gender-Specific effects govern susceptibility to Remitting/Relapsing (EAE12) and Monophasic Remitting/NonRelapsing (EAE7 and 13) EAE.
Authors Addresses
Univ of Illinois at Urbana-Champaign, Dept of Veterinary Pathobiology, Urbana, IL 61802
Allegheny Univ of the Health Sciences, Dept of Microbiology and Immunology, MCP-Hahnemann School of Medicine, Philadelphia, PA 19102
Purdue University, Depts of Agronomy and Statistics,
West Lafayette, IN 47907
Brigham Young University, Dept of Microbiology, Provo, UT 84602
Veterans Affairs Medical Center, NeuroVirology Research Laboratory,
Univ of Utah, Dept of Neurology, Salt Lake City, UT 84148
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