中华神经科杂志
中華神經科雜誌
중화신경과잡지
Chinese Journal of Neurology
2008年
2期
110-113
,共4页
吴怀国%杨毅%熊小平%许文华%任明山
吳懷國%楊毅%熊小平%許文華%任明山
오부국%양의%웅소평%허문화%임명산
重症肌无力,自身免疫性,实验性%鼻黏膜%免疫耐受%免疫接种,加强
重癥肌無力,自身免疫性,實驗性%鼻黏膜%免疫耐受%免疫接種,加彊
중증기무력,자신면역성,실험성%비점막%면역내수%면역접충,가강
Myasthenia gravis,autoimmune,experimental%Nasal mucosa%Immune tolerance%Immunization,secondary
目的 研究鼠源性乙酰胆碱受体α亚基97-116肽段丙氨酸替代108缬氨酸[Rα97-116(V108A)]鼻黏膜耐受对实验性自身免疫性重症肌无力(EAMG)大鼠肌无力表现及免疫功能的影响.方法 将采用Rα97-116强化免疫接种方法 成模的22只EAMG大鼠随机分成耐受组和对照组,分别经鼻黏膜给予Rα97-116(V108A)和PBS缓冲液免疫耐受处理10 d后,观察不同时间点两组大鼠体质量、Lennon肌无力评分、血清AChR-ab(ELISA法)及CD28、CTLA4、B7共刺激分子(流式细胞仪)变化.结果 耐受组EAMG大鼠体质量[(228.1±5.8)g]较对照组[(215.0±16.2)g]增加(t=2.395,P＜0.05);肌无力临床评分[耐受组(1.55±0.44)分,对照组(2.10士0.66)分]下降(t=-2.20,P＜0.05);血清AChR-ab(耐受组0.97±0.20,对照组1.27±0.26,t=-2.857,P＜0.05)和外周血CD28、B7-1、B7-2、CTLA4分子的表达(%)耐受组(分别为27.35±7.05、4.73±0.58、2.71±0.35、1.72±0.44)较对照组(分别为40.02±8.81、9.52±1.25、5.88±1.09、2.64±0.47)明显下调(t=3.479、10.861、8.755、4.403,均P＜0.01).结论 Rα97-116(V108A)鼻黏膜耐受能明显减轻EAMG的肌无力症状,并能引起特异性T细胞活化和B细胞免疫功能抑制.
目的 研究鼠源性乙酰膽堿受體α亞基97-116肽段丙氨痠替代108纈氨痠[Rα97-116(V108A)]鼻黏膜耐受對實驗性自身免疫性重癥肌無力(EAMG)大鼠肌無力錶現及免疫功能的影響.方法 將採用Rα97-116彊化免疫接種方法 成模的22隻EAMG大鼠隨機分成耐受組和對照組,分彆經鼻黏膜給予Rα97-116(V108A)和PBS緩遲液免疫耐受處理10 d後,觀察不同時間點兩組大鼠體質量、Lennon肌無力評分、血清AChR-ab(ELISA法)及CD28、CTLA4、B7共刺激分子(流式細胞儀)變化.結果 耐受組EAMG大鼠體質量[(228.1±5.8)g]較對照組[(215.0±16.2)g]增加(t=2.395,P＜0.05);肌無力臨床評分[耐受組(1.55±0.44)分,對照組(2.10士0.66)分]下降(t=-2.20,P＜0.05);血清AChR-ab(耐受組0.97±0.20,對照組1.27±0.26,t=-2.857,P＜0.05)和外週血CD28、B7-1、B7-2、CTLA4分子的錶達(%)耐受組(分彆為27.35±7.05、4.73±0.58、2.71±0.35、1.72±0.44)較對照組(分彆為40.02±8.81、9.52±1.25、5.88±1.09、2.64±0.47)明顯下調(t=3.479、10.861、8.755、4.403,均P＜0.01).結論 Rα97-116(V108A)鼻黏膜耐受能明顯減輕EAMG的肌無力癥狀,併能引起特異性T細胞活化和B細胞免疫功能抑製.
목적 연구서원성을선담감수체α아기97-116태단병안산체대108힐안산[Rα97-116(V108A)]비점막내수대실험성자신면역성중증기무력(EAMG)대서기무력표현급면역공능적영향.방법 장채용Rα97-116강화면역접충방법 성모적22지EAMG대서수궤분성내수조화대조조,분별경비점막급여Rα97-116(V108A)화PBS완충액면역내수처리10 d후,관찰불동시간점량조대서체질량、Lennon기무력평분、혈청AChR-ab(ELISA법)급CD28、CTLA4、B7공자격분자(류식세포의)변화.결과 내수조EAMG대서체질량[(228.1±5.8)g]교대조조[(215.0±16.2)g]증가(t=2.395,P＜0.05);기무력림상평분[내수조(1.55±0.44)분,대조조(2.10사0.66)분]하강(t=-2.20,P＜0.05);혈청AChR-ab(내수조0.97±0.20,대조조1.27±0.26,t=-2.857,P＜0.05)화외주혈CD28、B7-1、B7-2、CTLA4분자적표체(%)내수조(분별위27.35±7.05、4.73±0.58、2.71±0.35、1.72±0.44)교대조조(분별위40.02±8.81、9.52±1.25、5.88±1.09、2.64±0.47)명현하조(t=3.479、10.861、8.755、4.403,균P＜0.01).결론 Rα97-116(V108A)비점막내수능명현감경EAMG적기무력증상,병능인기특이성T세포활화화B세포면역공능억제.
Objective To study effect of nasal tolerance with rat-derived 97-116 peptide of AChR α-subunit(Rα97-116(V108A))on the manifestation of muscle weakness and the immunity function of experimental autoimmune myasthenia gravis(EAMG).Methods Twenty-two EAMG model Lewis rats immunized thrice with Rα97-116(V108A)were divided randomly into tolerance group and control group.They were respectively immunized with Rα97-116(V108A)and PBS buffer solution for 10 days via nasal mucous.Then the body weight and Lennon score of two group Lewis rats were measured.Their serum anti-AChR antibodies were tested by ELISA,the expression levels of CD28,CTLA4,B7-1 and B7-2 were determined by flow cytometry.Results Compared with control group at different time points.the body weight of tolerance group rats(tolerance group(228.1±5.8)g,control group(215.0±16.2)g,t=2.395,P＜0.05)increased,the mean clinical score of rats(tolerance group 1.55±0.44.control group 2.10±0.66,t=-2.20,P＜0.05)decreased and the amount of serum anti-AChR antibody(tolerance group 0.97±0.20,control group 1.27±0.26,t=-2.857,P＜0.05)decreased obviously.the amount of CD28,B7-1,B7-2,CTLA4(%)expressed on the surface of peripheral blood cells(tolerance group:27.35±7.05,4.73±0.58,2.71±0.35,1.72±0.44,control group:40.02±8.81,9.52±1.25,5.88±1.09,2.64±0.47)down-regulated markedly(t=3.479,10.861,8.755,4.403,all P＜0.01).Conclusion Nasal mucous tolerance with Rα97-116(V108A)could ameliorate muscular weakness of EAMG rats while activates T cell and inhibits B cellular immunity.
