TY - JOUR
T1 - Genetic Analysis of Disease Subtypes and Sexual Dimorphisms in Mouse Experimental Allergic Encephalomyelitis (EAE): Relapsing/remitting and Monophasic Remitting/nonrelapsing EAE Are Immunogenetically Distinct
AU - Butterfield, R.
AU - Blankenhorn, E.
AU - Roper, R.
AU - Zachary, J.
AU - Doerge, R.
AU - Sudweeks, Jayce
AU - Rose, J.
AU - Teuscher, C.
PY - 1999
Y1 - 1999
N2 - 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.
AB - 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.
KW - Disease subtypes
KW - EAE
KW - Genetic analysis
KW - Immunogenetically distinct
KW - Monophasic remitting/nonrelapsing
KW - Mouse experimental allergic encephalomyelitis
KW - Relapsing/remitting
KW - Sexual dimorphisms
UR - https://www.researchgate.net/publication/13217441_Genetic_analysis_of_disease_subtypes_and_sexual_dimorphisms_in_mouse_experimental_allergic_encephalomyelitis_EAE_Relapsingremitting_and_monophasic_remittingnonrelapsing_EAE_are_immunogenetically_disti
M3 - Article
VL - 162
JO - The Journal of Immunology
JF - The Journal of Immunology
ER -