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Topic: Experimental allergic encephalomyelitis

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	New Genetic Loci That Control Susceptibility and Symptoms of Experimental Allergic Encephalomyelitis in Inbred Mice -- ...
		Experimental allergic encephalomyelitis in inbred and outbred mice.
		Experimental allergic encephalomyelitis in congenic strains of mice.
		Neuropathology of experimental allergic encephalomyelitis in inbred strains of mice.
	www.jimmunol.org /cgi/content/full/161/4/1860 (5718 words)

	National MS Society \| Sourcebook: EAE (Site not responding. Last check: 2007-10-19)
		Experimental allergic encephalomyelitis (EAE), and the related experimental autoimmune encephalomyelitis, are diseases of the brain and spinal cord, similar in many respects to MS, which are induced in laboratory animals.
		Animals with EAE serve as animal models for MS, allowing experimentation that would be impossible and unethical in humans who have the disease.
		EAE is induced in strains of lab animals that are susceptible to the disease by injecting myelin or specific myelin proteins in combination with an immune-exciting agent, called an adjuvent.
	www.nationalmssociety.org /Sourcebook-EAE.asp (332 words)

	Oligodendrocyte cell death in pathogenesis of multiple sclerosis: Protection of oligodendrocytes from apoptosis by ... (Site not responding. Last check: 2007-10-19)
		In rats, EAE was ameliorated by depletion or inhibition of complement with cobra venom factor or soluble complement receptor 1 [59-60].
		Attenuation of experimental autoimmune demyelination in complement-deficient mice.
		Attenuation of experimental allergic encephalomyelitis in complement component 6-deficient rats is associated with reduced complement C9 deposition, P-selectin expression, and cellular infiltrate in spinal cords.
	www.vard.org /jour/06/43/1/cudrici.html (4344 words)

	experimental autoimmune encephalomyelitis - multiple sclerosis encyclopaedia (Site not responding. Last check: 2007-10-19)
		EAE is not multiple sclerosis, nor is it a single disease in a single species, but its different forms resemble the various forms and stages of MS very closely in a large number of ways.
		EAE is an acute or chronic-relapsing, acquired, inflammatory and demyelinating autoimmune disease.
		Because EAE is an animal disease, it enables researchers (especially immunologists) to study demyelination (the process underlying the symptoms of MS) in ways that would not be morally acceptable in studies of MS in humans.
	www.mult-sclerosis.org /experimentalautoimmuneencephalomyelitis.html (509 words)

	Office of Research Services (ORS) - Page Title (Site not responding. Last check: 2007-10-19)
		Inhibition of experimental allergic encephalomyelitis in the Lewis rat by paclitaxel.
		Dendritic cell-derived nitric oxide is involved in IL-4-induced suppression of experimental allergic encephalomyelitis (EAE) in Lewis rats.
		Cytokines and apoptotic molecules in experimental melanin-protein induced uveitis (EMIU) and experimental autoimmune uveoretinitis (EAU).
	dvrnet.ors.od.nih.gov /ratcenter/reference.html (4636 words)

	Steven M. LeVine, Ph.D. - Department of Molecular & Integrative Physiology, The University of Kansas Medical Center
		Emerson, MR, Orentas, DM, Lynch, SG and LeVine, SM (2002) Activation of histamine H 2 receptors ameliorates experimental allergic encephalomyelitis.
		Chakrabarty, A, Emerson, MR, and LeVine, SM (2003) Heme oxygenase-1 in SJL mice with experimental allergic encephalomyelitis.
		LeVine, SM and Chakrabarty, A (2004) The role of iron in the pathogenesis of experimental allergic encephalomyelitis and multiple sclerosis.
	www.kumc.edu /physiology/levine.html (397 words)

	Journal of Neuroinflammation \| Full text \| Experimental allergic encephalomyelitis in pituitary-grafted Lewis rats
		Experimental allergic encephalomyelitis (EAE) is one of best-studied models of autoimmune disease, and is characterized by an autoimmune attack on CNS myelin mediated by neural autoantigen-specific T helper cells [1].
		During induction of EAE, autoreactive T-cells are activated in the periphery by subcutaneous injection of either spinal cord homogenate (SCH) or CNS antigens, which may include myelin basic protein, myelin oligodendrocyte glycoprotein, or proteolipid protein or their peptides [2].
		Of relevance to EAE is the observation that treatment of animals with dopaminergic agonists which reduce prolactin release decreases both severity and duration of clinical signs of the disease [10,11].
	www.jneuroinflammation.com /content/3/1/20 (2265 words)

	Pathogenesis of Some Neurological Immune Diseases: Ultrastructural and Morphometrical Observations on Rat Thymus - ... (Site not responding. Last check: 2007-10-19)
		Experimental allergic encephalomyelitis (EAE) is a cell-mediated autoimmune disease of the central nervous system (CNS) characterized by inflammatory infiltrates and demyelination of the nervous tissues1,2.
		EAE was induced in adult Lewis rats by inoculation of an emulsion containing spinal cord tissue and Mycobacterium tuberculosis in complete Freund's adjuvant.
		Inhibition of experimental allergic encephalomyelitis with an antibody that recognizes a novel antigen expressed on lymphocytes, endothelial cells, and microglia.
	www.redorbit.com /news/display?id=125080 (3101 words)

	Oligodendrocyte cell death in pathogenesis of multiple sclerosis: Protection of oligodendrocytes from apoptosis by ...
		EAE is induced by immunization with myelin, myelin proteins, and myelin protein encephalitogenic epitopes or by the passive transfer of myelin-reactive cluster of differentiation (CD) 4 cells.
		In rats, EAE was ameliorated by depletion or inhibition of complement with cobra venom factor or soluble complement receptor 1 [59-60].
		Attenuation of experimental allergic encephalomyelitis in complement component 6-deficient rats is associated with reduced complement C9 deposition, P-selectin expression, and cellular infiltrate in spinal cords.
	www.rehab.research.va.gov /jour/06/43/1/Cudrici.html (4344 words)

	Dorlands Medical Dictionary
		It is characterized by destruction of the white matter to the point of liquefaction; widespread necrosis of blood vessel walls leading to the formation of multiple small hemorrhages in the involved areas and the exudation of fibrin into the surrounding tissue; and cellular infiltration of the necrotic areas.
		a type of encephalomyelitis in horses and mules, caused by an alphavirus and spread to humans by mosquitoes; it occurs in summer epizootics in the Western Hemisphere.
		(EAE) an animal model for acute disseminated encephalomyelitis in which the characteristic pathophysiology and clinical signs of this disease are produced by immunization of an animal with extracts of brain tissue or with myelin basic protein together with Freund's complete adjuvant; it is transferable by adoptive transfer of lymphocytes but not by serum.
	www.mercksource.com /pp/us/cns/cns_hl_dorlands.jspzQzpgzEzzSzppdocszSzuszSzcommonzSzdorlandszSzdorlandzSzdmd_e_07zPzhtm (3983 words)

	ePrintsUQ - The Pathophysiology of Acute Experimental Allergic Encephalomyelitis in the Rabbit
		ePrintsUQ - The Pathophysiology of Acute Experimental Allergic Encephalomyelitis in the Rabbit
		The Pathophysiology of Acute Experimental Allergic Encephalomyelitis in the Rabbit
		That the conduction block was due to demyelination was indicated by slowing of conduction in large diameter fibres, normal conduction in unmyelinated fibres and the specific effects of temperature and of the potassium channel blocking agent, 4-aminopyridine.
	eprint.uq.edu.au /archive/00003041 (321 words)

	ePrintsUQ - Vulnerability of the Dorsal Root Ganglion in Experimental Allergic Encephalomyelitis
		In recent studies on the pathophysiology of experimental allergic encephalomyelitis (EAE), the main animal model of multiple sclerosis, the DRG of the rabbit was shown to be the site of extensive inflammation and demyelination and of focal conduction block in a high proportion of the large diameter afferents.
		The vulnerability of the DRG is due to a deficient blood-nerve barrier and possibly also to a susceptibility of the branch point of the ganglion neurone to demyelination-induced conduction block.
		These and other studies in experimental animals suggest that in man the DRG may be a preferential (but neglected) site of focal structural and functional abnormalities in inflammatory and also other neurological diseases.
	eprint.uq.edu.au /archive/00000725 (257 words)

	Journal of Immune Based Therapies and Vaccines \| Full text \| Antigenized antibodies expressing Vbeta8.2 TCR peptides ...
		Experimental allergic encephalomyelitis (EAE) is an experimentally induced autoimmune disease mediated by T cells.
		Histologically, EAE is hallmarked by perivascular and submeningeal infiltration of inflammatory cells within the brain and spinal cord [4].
		EAE was shown to be prevented or attenuated by passive transfer of serum from rats recovering from EAE [52], or by passive transfer of monoclonal antibodies against these TCR Vβ region and its idiotypes [9,42-44].
	www.jibtherapies.com /content/2/1/9 (5414 words)

	Attenuation of Experimental Allergic Encephalomyelitis in Complement Component 6-Deficient Rats Is Associated with ...
		Attenuation of experimental autoimmune demyelination in complement-deficient mice.
		Soluble recombinant complement receptor 1 inhibits inflammation and demyelination in Ab-mediated demyelinating experimental allergic encephalomyelitis.
		Reversal of experimental allergic encephalomyelitis with non-mitogenic, non-depleting anti-CD3 mAb therapy with a preferential effect on T(h)1 cells that is augmented by IL-4.
	www.jimmunol.org /cgi/content/full/168/9/4293 (5755 words)

	Post-vaccinal encephalomyelitis
		This experimental allergic encephalomyelitis is mediated by sensitized lymphocytes rather than serum antibody mechanisms.
		Clinical suppression of experimental allergic encephalomyelitis by muramyl dipeptide "adjuvant".
		Schchelkunov, SN et al, "The Role of Viruses in the Induction of Allergic Encephalomyelitis," Dokl Akad Nauk SSSR, 1990,315(1):252-255.
	www.whale.to /vaccines/encephalomyelitis.html (1028 words)

	MK-801 Limits Neurovascular Dysfunction during Experimental Allergic Encephalomyelitis -- Bolton and Paul 282 (1): 397 ...
		Bolton, C. and Flower, R. The effects of the anti-glucocorticoid RU 38486 on steroid-mediated suppression of experimental allergic encephalomyelitis (EAE) in the Lewis rat.
		O'Neill, J. Baker, D., Davison, A. Maggon, K. Jaffee, B. and Turk, J. Therapy of chronic relapsing experimental allergic encephalomyelitis and the role of the blood-brain barrier: Elucidation by the action of Brequinar sodium.
		Paul, C. and Bolton, C.: Inhibition of blood-brain barrier disruption in experimental allergic encephalomyelitis by short-term therapy with dexamethasone or cyclosporin A. Int.
	jpet.aspetjournals.org /cgi/content/full/282/1/397 (3675 words)

	Studies of experimental allergic encephalomyelitis in old mice. (Site not responding. Last check: 2007-10-19)
		In old BALB/c mice susceptibility to experimental allergic encephalomyelitis (EAE) with bovine proteolipid apoprotein (PLP) is reduced significantly.
		Susceptibility to EAE induced by either PLP or bovine myelin basic protein (MBP) also was reduced in old SJL mice.
		In contrast, spleen cells from aged mice did not induce EAE, so the reduction of EAE susceptibility was mainly explained by the failure of T cell activity.
	www.arclab.org /medlineupdates/abstract_1698815.html (253 words)

	Dual phase regulation of experimental allergic encephalomyelitis by platelet-activating factor -- Kihara et al. 202 ...
		IL-6-deficient mice are resistant to the induction of experimental autoimmune encephalomyelitis provoked by myelin oligodendrocyte glycoprotein.
		IL-6-deficient mice are resistant to experimental autoimmune encephalomyelitis: roles of IL-6 in the activation and differentiation of autoreactive T cells.
		Induction of experimental autoimmune encephalomyelitis in IL-12 receptor-beta 2-deficient mice: IL-12 responsiveness is not required in the pathogenesis of inflammatory demyelination in the central nervous system.
	www.jem.org /cgi/content/full/202/6/853 (6566 words)

	Bibliographic Database
		Apoferritin Attenuates Experimental Allergic Encephalomyelitis in SJL Mice
		Amelioration of experimental autoimmune encephalomyelitis in C57BL/6 mice by an agonist of peroxisome proliferator-activated receptor- gamma
		Sodium fusidate (fusidin) ameliorates the course of monophasic experimental allergic encephalomyelitis in the Lewis rat
	content.csa.com /biblio/BSS000043.html (4683 words)

	Disease Progression in Chronic Relapsing Experimental Allergic Encephalomyelitis Is Associated with Reduced ...
		By 17 d.p.i., animals suffering from EAE and healthy controls (n = 8 in each group) were subjected to either a mild psychological stimulus (30 min of novelty stress) (A and B) or an inflammatory stimulus (ip injection of rat IL-1ß) (C and D).
		1994 Identification of epitopes of myelin oligodendrocyte glycoprotein for the induction of experimental allergic encephalomyelitis in SJL and Biozzi AB/H mice.
		1999 Myelin oligodedrocyte glycoprotein induces experimental autoimmune encephalomyelitis in the "resistant" brown Norway rat: disease susceptibility is determined by MHC and MHC-linked effects on the B-cell response.
	endo.endojournals.org /cgi/content/full/142/8/3616 (5298 words)

	Allergy & Asthma Disease Management Center: Ask the Expert
		There seems to be a lot of literature on experimental allergic encephalitis in mice, and case reports of allergic encphalitis after vaccination.
		The word "allergic" was included in the term "experimental allergic encephalomyelitis (EAE)" early in the use of this experimental model even though there is no evidence that IgE-mediated allergic responses play a pathogenic role.
		The post-infectious and post-vaccination acute encephalomyelitis in humans also appears to be mainly T cell mediated with no evidence that I know for an IgE mediation.
	www.aaaai.org /aadmc/ate/category.asp?cat=1048 (376 words)

	Susceptibility and Resistance to Experimental Allergic Encephalomyelitis: Relationship with ...
		EAE is associated with HPA axis activation in susceptible strains.
		to EAE is in stark contrast to its robust HPA axis response.
		Williams RM, Moore MJ 1973 Linkage of susceptibility to experimental allergic encephalomyelitis to the major histocompatibility locus in the rat.
	endo.endojournals.org /cgi/content/full/140/11/4932 (5387 words)

	Experimental Allergic Encephalomyelitis Cancer Related Definition
		Definition: An autoimmune demyelinating disease of the central nervous system that is produced experimentally in animals by the injection of homogenised brain or spinal cord in Freund's adjuvant.
		Myelin basic protein appears to be the antigen that elicits the hypersensitivity immune response which is characterized by focal areas of lymphocyte and macrophage infiltration into the brain, associated with demyelination and destruction of the blood-brain barrier.
		Experimental allergic encephalomyelitis (EAE) is used as an animal model for demyelinating diseases of the human central nervous system such as multiple sclerosis.
	www.thenutritionguide.com /nci/2803.html (131 words)

	Modulation of Blood-Brain Barrier Dysfunction and Neurological Deficits during Acute Experimental Allergic ...
		EAE-inoculated animals in each experimental group were assessed on day 12 PI for alterations in BBB permeability (A) and on days 10 to 12 PI for the development of neurological disease (B).
		EAE-inoculated animals in each experimental group were assessed on day 12 PI for changes in BBB permeability (A) and on days 10 to 12 PI for the development of neurological EAE (B).
		Scott GS, Williams KI and Bolton C (1996) A pharmacological study on the role of nitric oxide in the pathogenesis of experimental allergic encephalomyelitis.
	jpet.aspetjournals.org /cgi/content/full/302/1/50 (4328 words)

	The immunopathology of acute experimental allergic encephalomyelitis induced with myelin proteolipid protein. T cell ...
		The immunopathology of acute experimental allergic encephalomyelitis induced with myelin proteolipid protein.
		tissues of mice with experimental allergic encephalomyelitis (EAE).
		EAE was induced in SJL/J mice either by sensitization with a synthetic
	www.jimmunol.org /cgi/content/abstract/149/4/1444 (827 words)

	ePrintsUQ - Recovery from Acute Experimental Allergic Encephalomyelitis in the Lewis Rat: Early Restoration of Nerve ...
		Recovery from Acute Experimental Allergic Encephalomyelitis in the Lewis Rat: Early Restoration of Nerve Conduction and Repair by Schwann Cells and Oligodendrocytes
		Light and electron microscopic histological studies and electrophysiological studies were performed on Lewis rats with acute experimental allergic encephalomyelitis (EAE) induced by whole spinal cord or myelin basic protein to determine the mechanism of clinical recovery.
		Citation: MP Pender, Recovery from acute experimental allergic encephalomyelitis in the Lewis rat.
	eprint.uq.edu.au /archive/00002891 (263 words)

	Analysis of T cell receptor beta chains in Lewis rats with experimental allergic encephalomyelitis: conserved ...
		Analysis of T cell receptor beta chains in Lewis rats with experimental allergic encephalomyelitis: conserved complementarity determining region 3 -- Gold et al.
		Analysis of T cell receptor beta chains in Lewis rats with experimental allergic encephalomyelitis: conserved complementarity determining region 3
		Okura, Y., Jee, Y., Matsumoto, Y. Acquired thymic tolerance to autoimmune encephalomyelitis is associated with activation of peripheral IL-10-producing macrophages/dendritic cells.
	www.jem.org /cgi/content/abstract/174/6/1467 (934 words)

	Recovery from experimental allergic encephalomyelitis is TGF-{beta} dependent and associated with increases in CD4+LAP+ ...
		hallmark of EAE is a perivascular infiltrate in the CNS comprising
		Immunization with PLP 139–151 induces EAE in SJL mice.
		Khoury, S. J., Hancock, W. and Weiner, H. Oral tolerance to myelin basic protein and natural recovery from experimental autoimmune encephalomyelitis are associated with downregulation of inflammatory cytokines and differential upregulation of transforming growth factor beta, interleukin 4, and prostaglandin E expression in the brain.
	intimm.oxfordjournals.org /cgi/content/full/18/4/495 (4639 words)

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