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關(guān)鍵詞：多發(fā)性硬化癥,，Multiple sclerosis,，EAE，MOG, MOG35-55,，PLP,，PLP (139-151)，實(shí)驗(yàn)性自身免疫性腦脊髓炎

多發(fā)性硬化癥（Multiple sclerosis (MS)）/實(shí)驗(yàn)性自身免疫性腦脊髓炎模型（EAE）研究專題

背景介紹

多發(fā)性硬化癥(multiple sclerosis, MS)是一種原發(fā)于中樞神經(jīng)系統(tǒng)的炎癥性脫髓鞘疾病,。MS確切的發(fā)病機(jī)制雖尚不清楚, 但普遍認(rèn)為是在易感基因的基礎(chǔ)上, 受環(huán)境因素觸發(fā), 由CD4⁺ T細(xì)胞介導(dǎo)的中樞神經(jīng)系統(tǒng)(central nervous system, CNS)自身免疫性疾病,。實(shí)驗(yàn)性自身免疫性腦脊髓炎(experimental autoimmune encephalomyelitis, EAE)是一種以特異性致敏的CD4⁺ T細(xì)胞介導(dǎo)為主, 對(duì)實(shí)驗(yàn)動(dòng)物進(jìn)行髓鞘蛋白免疫構(gòu)建的疾病模型。EAE與人類MS在臨床,、生化,、免疫及病理等諸多方面具有相同的特征, 所以它是目前*的 MS理想動(dòng)物模型。

（一）慢性EAE（Chronic EAE）模型的建立

髓鞘少突膠質(zhì)細(xì)胞糖蛋白(MOG) 是髓鞘膜和少突膠質(zhì)細(xì)胞表面zui外層的膜蛋白,，是導(dǎo)致多發(fā)性硬化（MS）脫髓鞘的關(guān)鍵成分,，針對(duì)MOG的抗體能夠在體內(nèi)和體外造成脫髓鞘。MOG數(shù)量較少,，約占髓鞘蛋白總量的0.01%-0.05%,，具有高度免疫原性，它直接參與CNS的體液免疫反應(yīng),，是引起實(shí)驗(yàn)性自身免疫性腦脊髓炎（EAE）中脫髓鞘的主要免疫靶點(diǎn),。MOG 35-55含21個(gè)氨基酸，是*既能引起脫髓鞘抗體反應(yīng)又能引起T細(xì)胞反應(yīng)的中樞神經(jīng)系統(tǒng)髓鞘蛋白成分,。MOG 35-55可在C57BL/6小鼠體內(nèi)誘導(dǎo)MOG35-55/I-Ab特異性自身反應(yīng)性CD4⁺T細(xì)胞異?；罨T發(fā)EAE,。

產(chǎn)品性質(zhì)

運(yùn)輸與保存方法

冰袋（wet ice）運(yùn)輸,。收到產(chǎn)品后放到-20 oC保存，保持干燥,。不建議溶液狀態(tài)保存,。

產(chǎn)品信息

Q&A

1. 如何選擇模型動(dòng)物？

答：一般選擇雌性C57BL/6小鼠,，10-14周左右,。

2.在什么部位注射？每次注射的量,？

皮下注射,，每只小鼠200μg MOG 35-55多肽。

參考文獻(xiàn)

1.Mandy?L. Ford, et al. An MHC anchor-substituted analog of myelin oligodendrocyte glycoprotein?35–55 induces IFN-γ and autoantibodies in the absence of experimental autoimmune encephalomyelitis and optic neuritis. European Journal of Immunology Volume 34, Issue 2, pages 388–397,February 2004

2.Cathleen Rich, et al. Myelin oligodendrocyte glycoprotein-35–55 peptide induces severe chronic experimental autoimmune encephalomyelitis in HLA-DR2-transgenic mice. Eur. J. Immunol. 2004. 34: 1251–1261

3.Cong-Qiu Chu, et al. Failure to Suppress the Expansion of the Activated Cd4 T Cell Population in Interferon γ–Deficient Mice Leads to Exacerbation of Experimental Autoimmune Encephalomyelitis. JEM Home 2000 Archive 3 July Chu et al. 192 (1): 123.

4. Stefanie Kuerten, et al. MP4- and MOG:35–55-induced EAE in C57BL/6 mice differentially targets brain, spinal cord and cerebellum. Journal of Neuroimmunology Volume 189, Issues 1–2, 2007 (31–40).

5. Anthony Slavin, et al. Induction of a Multiple Sclerosis-Like Disease in Mice with an Immunodominant Epitope of Myelin Oligodendrocyte Glycoprotein. 1998, Vol. 28, No. 2 , 109-120.

6. McFarland, H. F., et al. Multiple sclerosis: a complicated picture of autoimmunity. Nat. Immunol. 8, 913-919, doi:10.1038/ni1507

(2007).

7. Wiendl, H. Neuroinflammation: the world is not enough. Curr. Opin. Neurol. 25, 302-305, doi:10.1097/WCO.0b013e3283534abf (2012).

8. van der Star, B. J. et al. In vitro and in vivo models of multiple sclerosis. CNS Neurol. Disord. Drug Targets. 11, 570-588 (2012).

9. Pachner, A. R. Experimental models of multiple sclerosis. Curr. Opin. Neurol. 24, 291-299, doi:10.1097/WCO.0b013e328346c226 (2011).

10. Bittner, S. et al. The TASK1 channel inhibitor A293 shows efficacy in a mouse model of multiple sclerosis. Exp. Neurol. 238, 149-155, doi:10.1016/j.expneurol.2012.08.021 (2012).

（二）復(fù)發(fā)-緩解型EAE（Relapsing- Remitting EAE）模型的建立

復(fù)發(fā)-緩解型MS是人類多發(fā)性硬化（MS）zui常見(jiàn)的一種,，這類型的疾病與PLP_139-151/CFA誘導(dǎo)的SJL小鼠EAE癥狀zui為相似,，因此,，這是一種常用于研究藥物對(duì)復(fù)發(fā)型EAE作用的模型。而且,，該模型也表現(xiàn)出較高的EAE同步發(fā)病率,。復(fù)發(fā)-緩解型EAE常用于MS治療，以研究EAE復(fù)發(fā)的進(jìn)展情況,。Proteolipid Protein (PLP)是一種高度疏水的膜蛋白,，是中樞神經(jīng)系統(tǒng)(central nervous system, CNS)中含量zui多的髓磷脂。與IA^S MHCII結(jié)合時(shí),，PLP 139–151和PLP 178–191具有相同的高親和力,，但是，免疫系統(tǒng)對(duì)PLP 139–151表位產(chǎn)生的免疫反應(yīng)是主要的,。對(duì)于PLP誘導(dǎo)的EAE模型,，SJL (H-2^s)小鼠具有很高的致敏性,。

產(chǎn)品性質(zhì)

運(yùn)輸與保存方法

冰袋（wet ice）運(yùn)輸,。收到產(chǎn)品后放到-20 oC保存，保持干燥,。不建議溶液狀態(tài)保存,。

產(chǎn)品信息

Direct EAE induction in SJL mice

Q&A

1. 如何選擇模型動(dòng)物？

答：一般選擇雌性SJL小鼠,，9-10周左右,。

2.在什么部位注射？每次注射的量,？

皮下注射,，每只小鼠100μg PLP_139-151 。

參考文獻(xiàn)

1. McRae BL, et al. Differential recognition of peptide analogs by naive verses activated PLP 139-151-specific CD4+ T cells. J Neuroimmunol. 1995 Jul;60(1-2):17-28.

2. Ana C. Anderson, et al. High Frequency of Autoreactive Myelin Proteolipid Protein–Specific T Cells in the Periphery of Naive Mice. JEM vol. 191 (5): 761-770.

3. Maria Katsara, et al. Immune responses of linear and cyclic PLP139-151 mutant peptides in SJL/J mice: peptides in their free state versus mannan conjugation. Immunotherapy, 6(6): 709-724. DOI 10.2217/imt.14.42

4. Stephen D. Miller, et al. Experimental Autoimmune Encephalomyelitis in the Mouse. Curr Protoc Immunol. 2007 May ; CHAPTER: Unit–15.1. doi:10.1002/0471142735.im1501s77.

5. Hanspeter Waldner, et al. Fulminant spontaneous autoimmunity of the central nervous system in mice transgenic for the myelin proteolipid protein-specific T cell receptor. PNAS March 28, 2000 97(7) 3412–3417.

6. By Ana C. Anderson, et al. High Frequency of Autoreactive Myelin Proteolipid Protein–specific T Cells in the Periphery of Naive Mice: Mechanisms of Selection of the Self-reactive Repertoire. J. Exp. Med. 191(5) 2000: 761–770.

7. Harald H. Hofstetter, et al. 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 2002; 169:117-125.