関: allergic encephalomyelitis、EAE、experimental allergic encephalomyelitis

WordNet

to conduct a test or investigation; "We are experimenting with the new drug in order to fight this disease"
the act of conducting a controlled test or investigation (同)experimentation
a venture at something new or different; "as an experiment he decided to grow a beard"
the testing of an idea; "it was an experiment in living"; "not all experimentation is done in laboratories" (同)experimentation
try something new, as in order to gain experience; "Students experiment sexually"; "The composer experimented with a new style" (同)try out
relating to or based on experiment; "experimental physics"
relying on observation or experiment; "experimental results that supported the hypothesis" (同)data-based, observational
of the nature of or undergoing an experiment; "an experimental drug"
of or relating to the immune response of the body against substance normally present in the body
inflammation of the brain and spinal cord

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(…の)『実験』,試み《+『in』(『on, with』)+『名』》 / (…の)実験をする《+『on(upon, with)』+『名』》
実験の,実験に基づく: / 実験に使われる,実験用の / 実験的な,試験的な

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/10/26 21:23:37」(JST)

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The experimental autoimmune encephalomyelitis, sometimes experimental allergic encephalomyelitis (EAE) is an animal model of brain inflammation. It is an inflammatory demyelinating disease of the central nervous system (CNS). It is mostly used with rodents and is widely studied as an animal model of the human CNS demyelinating diseases, including multiple sclerosis and acute disseminated encephalomyelitis (ADEM). EAE is also the prototype for T-cell-mediated autoimmune disease in general.

EAE was motivated by observations during the convalescence from viral diseases by Thomas M. Rivers, D. H. Sprunt and G. P. Berry in 1933. Their findings upon a transfer of inflamed patient tissue to primates was published in the Journal of Experimental Medicine (Vol. 58, No. 1, pp. 39–56).^[1]^[2] An acute monophasic illness, it has been suggested that EAE is far more similar to ADEM than MS.^[3]

EAE can be induced in a number of species, including mice, rats, guinea pigs, rabbits and primates. The most commonly used antigens in rodents are spinal cord homogenate (SCH), purified myelin, myelin protein such as MBP, PLP and MOG, or peptides of these proteins, all resulting in distinct models with different disease characteristics regarding both immunology and pathology.^[4]^[5] It may also be induced by the passive transfer of T cells specifically reactive to these myelin antigens^{[citation needed]}. Depending on the antigen used and the genetic make-up of the animal, rodents can display a monophasic bout of EAE, a relapsing-remitting form, or chronic EAE . The typical susceptible rodent will debut with clinical symptoms around two weeks after immunization and present with a relapsing-remitting disease. The archetypical first clinical symptom is weakness of tail tonus that progresses to paralysis of the tail, followed by a progression up the body to affect the hind limbs and finally the forelimbs. However, similar to MS, the disease symptoms reflect the anatomical location of the inflammatory lesions, and may also include emotional lability, sensory loss, optic neuritis, difficulties with coordination and balance (ataxia), and muscle weakness and spasms. Recovery from symptoms can be complete or partial and the time varies with symptoms and disease severity. Depending on the relapse-remission intervals, rats can have up to 3 bouts of disease within an experimental period.

EAE in mice[edit]

Demyelination is produced by injection of brain extracts, CNS proteins (such as myelin basic protein), or peptides from such protein emulsified in an adjuvant such as complete Freund's adjuvant. The presence of the adjuvant allows the generation of inflammatory responses to the protein/peptides. In many protocols, mice are coinjected with pertussis toxin to break down the blood-brain barrier and allow immune cells access to the CNS tissue. This immunisation leads to multiple small disseminated lesions of demyelination (as well as micro-necroses) in the brain and spinal cord and the onset of clinical symptoms.

Although sharing some features, mostly demyelination, this model, first introduced in 1930s, differs from human MS in several ways. EAE either kills animals or leaves them with permanent disabilities; animals with EAE also suffer severe nerve inflammation, and the time course of EAE is entirely different from MS, being the main antigen (MBP) in charge.

Notes and references[edit]

^ Rivers TM, Spunt DH & Berry GP (1933). OBSERVATIONS ON ATTEMPTS TO PRODUCE ACUTE DISSEMINATED ENCEPHALOMYELITIS IN MONKEYS. Journal of Experimental Medicine 58:39-53.
^ Rivers TM & Schwentker FF. (1935). Encephalomyelitis accompanied by myelin destruction experimentally produced in monkeys. Journal of Experimental Medicine 61:689 –701.
^ Sriram S & Steiner I (2005) Experimental Allergic Encephalomyelitis: A misleading model of Multiple Sclerosis. Annals of Neurology 58:939 –945.
^ MANNIE, M., R. H. SWANBORG and J. A. STEPANIAK, 2009 Experimental autoimmune encephalomyelitis in the rat. Curr Protoc Immunol Chapter 15: Unit 15 12
^ MILLER, S. D., and W. J. KARPUS, 2007 Experimental autoimmune encephalomyelitis in the mouse. Curr Protoc Immunol Chapter 15: Unit 15 11

External links[edit]

Mult-sclerosis.org: information on EAE
More than 100, freely available, published research articles on EAE and related topics such as multiple sclerosis by Professor Michael P. Pender, Neuroimmunology Research Unit, The University of Queensland

UpToDate Contents

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English Journal

K(+) channel alterations in the progression of experimental autoimmune encephalomyelitis.

Jukkola PI, Lovett-Racke AE, Zamvil SS, Gu C.SourceIntegrated Biomedical Graduate Program, The Ohio State University, Columbus, OH, 43210, USA.
Neurobiology of disease.Neurobiol Dis.2012 Aug;47(2):280-93. Epub 2012 Apr 24.
Voltage-gated K(+) (Kv) channels play critical roles not only in regulating synaptic transmission and intrinsic excitability of neurons, but also in controlling the function and proliferation of other cells in the central nervous system (CNS). The non-specific Kv channel blocker, 4-AminoPyridine (4-
PMID 22560931

In vitro screening of NADPH oxidase inhibitors and in vivo effects of L-leucinethiol on experimental autoimmune encephalomyelitis-induced mice.

Kandagaddala LD, Kang MJ, Haque MM, Im HY, Seo JE, Chung BC, Jung BH, Patterson TA, Kwon OS.SourceToxicology Laboratory, Korea Institute of Science and Technology, Seoul 136-791, Republic of Korea; Biomolecular Sciences, University of Science and Technology, Daejon 305-333, Republic of Korea.
Journal of the neurological sciences.J Neurol Sci.2012 Jul 15;318(1-2):36-44. Epub 2012 May 2.
Experimental autoimmune encephalomyelitis (EAE), a Th1 polarized demyelinating disease of the central nervous system, shares many pathological and clinical similarities with multiple sclerosis (MS). The objectives of this study were i) to evaluate the suppressive effects of l-leucinethiol (LeuSH), a
PMID 22554692

Japanese Journal

Programmed cell death 1 inhibits inflammatory helper T-cell development through controlling the innate immune response

Rui Yuxiang,Honjo Tasuku,Chikuma Shunsuke
Proceedings of the National Academy of Sciences of the United States of America, 2013-09-16
… 2013-09-17.Programmed cell death 1 (PD-1) is an inhibitory coreceptor on immune cells and is essential for self-tolerance because mice genetically lacking PD-1 (PD-1(-/-)) develop spontaneous autoimmune diseases. … PD-1(-/-) mice are also susceptible to severe experimental autoimmune encephalomyelitis (EAE), characterized by a massive production of effector/memory T cells against myelin autoantigen, the mechanism of which is not fully understood. …
NAID 120005324915

An Overview of Models, Methods, and Reagents Developed for Translational Autoimmunity Research in the Common Marmoset (Callithrix jacchus)

Jagessar S. Anwar,Vierboom Michel,Blezer Erwin L.A.,Bauer Jan,Hart Bert A. 't,Kap Yolanda S.
Experimental
… The common marmoset (Callithrix jacchus) is a small-bodied Neotropical primate and a useful preclinical animal model for translational research into autoimmune-mediated inflammatory diseases (AIMID), such as rheumatoid arthritis (RA) and multiple sclerosis (MS). …
NAID 130003362953

制御性B細胞におけるSTIM依存的カルシウム流入の役割

松本真典,馬場義裕
YAKUGAKU ZASSHI 133(4), 419-425, 2013
… We have recently found that STIM1- and STIM2-induced SOC influx is critical for regulatory B cell function required to limit experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis. … Even through several B cell populations have been reported to suppress inflammation of autoimmune diseases through production of IL-10, which subset of them exerts their regulatory function during EAE is not fully understood. …
NAID 130003361933

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★リンクテーブル★

リンク元	「EAE」「実験的自己免疫性脳脊髄炎」「allergic encephalomyelitis」
関連記事	「experimental」「experiment」「experimental autoimmune」