Experimental autoimmune encephalomyelitis - achievements and prospective advances

被引:63
作者
Batoulis, Helena [1 ]
Recks, Mascha S. [1 ]
Addicks, Klaus [1 ]
Kuerten, Stefanie [1 ]
机构
[1] Univ Cologne, Dept Anat 1, D-50931 Cologne, Germany
关键词
Autoantibodies; B cells; EAE; MS; spontaneous; T(H)1/T(H)17;
D O I
10.1111/j.1600-0463.2011.02794.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
Multiple sclerosis (MS) is an autoimmune disorder of the CNS. Different subtypes of the disease have been noted, and characterized by distinct clinical courses and histopathologic manifestations. The most intensively studied animal model of MS, experimental autoimmune encephalomyelitis (EAE), classically leads to deficits in motor functions, and is mediated by T helper cells. Recently, T(H)17 cells were ascribed an even greater pathogenic impact than T(H)1 cells, but new findings render this view controversial. Although classic EAE has been an invaluable tool, it does not cover the entire pathogenic entity of MS. Especially B-cell contribution and autoantibody-dependence are not mirrored adequately: therefore, new B-cell-dependent models, such as MP4-induced EAE, have been introduced. Furthermore, certain symptoms and the spontaneous onset of MS are not featured in classic EAE. Herein, atypical and spontaneous EAE models can be used for investigation of common symptoms, such as tremor and ataxia, as well as spontaneous disease development. MS displays a marked inter-individual heterogeneity, and no single model will be able to cover all features. Thus, depending on the objective of one's study, the appropriate EAE model has to be carefully chosen. In addition, refined models should be designed to gain a more complete understanding of MS.
引用
收藏
页码:819 / 830
页数:12
相关论文
共 88 条
[1]
Dyment D.A., Ebers G.C., Sadovnick A.D., Genetics of multiple sclerosis, Lancet Neurol, 3, pp. 104-110, (2004)
[2]
Sospedra M., Martin R., Immunology of multiple sclerosis, Annu Rev Immunol, 23, pp. 683-747, (2005)
[3]
Soldan S.S., Jacobson S., Role of viruses in etiology and pathogenesis of multiple sclerosis, Adv Virus Res, 56, pp. 517-555, (2001)
[4]
Ascherio A., Munger K.L., Simon K.C., Vitamin D and multiple sclerosis, Lancet Neurol, 9, pp. 599-612, (2010)
[5]
Hillert J., Olerup O., HLA and MS, Neurology, 43, pp. 2426-2427, (1993)
[6]
Fogdell-Hahn A., Ligers A., Gronning M., Hillert J., Olerup O., Multiple sclerosis: a modifying influence of HLA class I genes in an HLA class II associated autoimmune disease, Tissue Antigens, 55, pp. 140-148, (2000)
[7]
Kipp M., Clarner T., Dang J., Copray S., Beyer C., The cuprizone animal model: new insights into an old story, Acta Neuropathol, 118, pp. 723-736, (2009)
[8]
Tsunoda I., Fujinami R.S., Neuropathogenesis of Theiler's murine encephalomyelitis virus infection, an animal model for multiple sclerosis, J Neuroimmune Pharmacol, 5, pp. 355-369, (2010)
[9]
Rivers T.M., Sprunt D.H., Berry G.P., Observations on attempts to produce acute disseminated encephalomyelitis in monkeys, J Exp Med, 58, pp. 39-53, (1933)
[10]
Hofstetter H.H., Shive C.L., Forsthuber T.G., Pertussis toxin modulates the immune response to neuroantigens injected in incomplete Freund's adjuvant: induction of Th1 cells and experimental autoimmune encephalomyelitis in the presence of high frequencies of Th2 cells, J Immunol, 169, pp. 117-125, (2002)