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ID:28568045
大小:10.75 MB
页数:59页
时间:2018-12-11
《ifnγ及il33在ean中的表达及p2 5873aaimdc干预对其表达的影响》由会员上传分享,免费在线阅读,更多相关内容在应用文档-天天文库。
1、硕士学位论文中文摘要目的初步探讨P258—73aa—iMDC对EAN的干预效果及IFN-Y及IL一33在EAN发病机制中可能起到的作用方法.1.随机分组为四组:CFA对照组(A组)一第一7天背部皮下注射lmlPBS,第O天双后肢足垫皮内注射200I_qCFA乳剂;EAN组(B组)一第.7天背部皮下注射lml0.1MPBS,第0天双后肢足垫皮内注射200“1抗原乳剂;iMDC组(C组)·.第一7天背部皮下注射含3×106个/mliMDC的PBSlml,第0天双后肢足垫皮内注射200I_tl抗原乳剂;P2
2、58—73aa-iMDC组(D组)一第.7天背部皮下注射含3×106个/rrflP258.73aa.iMDC的PBSlml,第0天双后肢足垫皮内注射200rq抗原乳剂。2.取大鼠骨髓干细胞培养髓源未成熟DC及用P258-73缸负载未成熟的DC。3.制作EAN模型:以近交系SPF级Lewis大鼠为动物模型对象,双后肢足垫皮内注射200I.q抗原乳剂(由含100}tgP253-78缸的100J.qO.1MPBS和100J_tlCFA用针式匀浆器混匀成油包水乳剂)一次,免疫均在腹腔注射10%水合氯醛(O.3
3、—0.4mg/1009)后数分钟,麻醉满意时进行。4.结束临床观察时,分别取双侧坐骨神经组织、淋巴组织j脾组织‘待下步处理。5.取坐骨神经根制作石蜡切片,行HE染色并于光镜下观察。6.取部分引流淋巴结行淋巴细胞抗原特异性增殖反应。7.RT-PCR法半定量分别检测四组大鼠坐骨神经组织、脾组织及淋巴n硕士学位论文中文摘要组织IFN.Y和几一33mRNA的表达量。结果1.与EAN组相比,P258.73aa.iMDC组大鼠的临床表现均明显减轻。2..与EAN组相比,P258.73aa-iMDC组大鼠的坐骨神经
4、组织炎性细胞浸润情况及脱髓鞘情况明显好转。3.与EAN组相比,在淋巴细胞体外增殖反应中,P258.73aa.iMDC可抑制抗原特异性T细胞增殖(p5、过抑制IFN—Y的分泌,解除对几.33分泌的抑制而诱导免疫耐受。关键词EAN,P258.73aa-iMDC,IFN-Y,IL一331/I硕士学位论文英文摘要ABSTRACTBackgroundGuilliam-Barresyndromeisregardedasakindofautoimmuneperipheralneuropathies.NowthepathogenesisofGBSremainspoorlyunderstood.Manyresearcherst11iIlkmoleculermimic6、kingisanimportantpathomechanismforGBS.Inthishypothesis,thepartofcomponentsofpathogenissimilartosomeperipheralnervecomponents,whichleadtOtheimmunologictOlerancetOthesecomponentsislost,andinducetheautoimmunereactivitymediatedbyspecificantibodiesorautoreac7、tiveTlymphocytesNowthebesttherapiesfortheGBSareplasmaexchangeandintravenousimmunoglobulin.Unfortunately,Itiseffectiveforaboutonethirdcasesandmayresultinmuchsideeffect,SOthemostperfecttheraphyforthediseaseistOinducetheantigenspecificimmunologictolerance.8、ObjectToinvestigatetheinterferingeffectofP258..73aa.-iMDCforEANandtOdiscusswhetherornottheIFN--gammaandtheIL--33contributealottOthepathomechanismoftheEAN.Methods1.Grouping:28Lewisratsweredividedintofourrandomizedgroups,whichwerec
5、过抑制IFN—Y的分泌,解除对几.33分泌的抑制而诱导免疫耐受。关键词EAN,P258.73aa-iMDC,IFN-Y,IL一331/I硕士学位论文英文摘要ABSTRACTBackgroundGuilliam-Barresyndromeisregardedasakindofautoimmuneperipheralneuropathies.NowthepathogenesisofGBSremainspoorlyunderstood.Manyresearcherst11iIlkmoleculermimic
6、kingisanimportantpathomechanismforGBS.Inthishypothesis,thepartofcomponentsofpathogenissimilartosomeperipheralnervecomponents,whichleadtOtheimmunologictOlerancetOthesecomponentsislost,andinducetheautoimmunereactivitymediatedbyspecificantibodiesorautoreac
7、tiveTlymphocytesNowthebesttherapiesfortheGBSareplasmaexchangeandintravenousimmunoglobulin.Unfortunately,Itiseffectiveforaboutonethirdcasesandmayresultinmuchsideeffect,SOthemostperfecttheraphyforthediseaseistOinducetheantigenspecificimmunologictolerance.
8、ObjectToinvestigatetheinterferingeffectofP258..73aa.-iMDCforEANandtOdiscusswhetherornottheIFN--gammaandtheIL--33contributealottOthepathomechanismoftheEAN.Methods1.Grouping:28Lewisratsweredividedintofourrandomizedgroups,whichwerec
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