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作 者:高建新[1,2] 马宝骊[1,2] 谢雅莉[1,2] 张汉明[1,2]
机构地区:[1]上海第二医科大学免疫学教研室 [2]上海市免疫学研究所基础免疫研究一室
出 处:《上海免疫学杂志》1993年第4期193-196,共4页Shanghai Journal of Immunology
基 金:国家自然科学基金;卫生部资助
摘 要:空肠弯曲菌(CJ-S131)感染昆明(KM)小鼠后15个月,KM小鼠仍然具有并发展了感染后3个月所表现的自身免疫综合征。其表现为抗核抗体阳性;多种自身抗体(抗ds-DNA,ss-DNA,组蛋白,ENA和胸腺细胞抗体)升高;肠淋巴组织增生,胸腺呈纤维化倾向,脾脏、淋巴结肿大;免疫复合物性肾小球肾炎和血管炎;肠道及肠外多器官(肝脏、肺、心脏和唾液腺等)慢性炎症;空弯菌外膜蛋白(CJ-OMP)特异性抗体与自身抗体的消长相背离,随感染时间延长,CJ-OMP抗体阳性百分率下降,抗ds-DNA,ENA和胸腺细胞等抗体的阳性率上升。本文再次证实,慢性空弯菌感染可诱发小鼠自身免疫综合征,而诱发因子特异性抗体随自身免疫综合征的出现而下降。Kun-Ming (KM) mice chronically infected for 15 months demonstrated autoimmune syndrome (1-4), which was characterized by (1) severe glomerulonephritis with large quantity of protein in the urine and deposits of IgA and IgG in the glome-ruli; (2) chronic inflammation in multiple organs such as intestine, liver, lung, heart, salivary gland and blood vessels, infiltrated with mononuclear and lymphoid cells; (3) prominent lymphoproliferation; (4) high titer of autoantibodies against ds-DNA, ss-DNA, histones, extractable nuclear antigens (ENA) and thymocytes. Plow-ever, the CJ-OMP (outer membrane proteins of C. jejuni) specific antibody reduced gradually while autoantibody titers going up continuously as time passed(in this study, up to 15 months). The results confirmed that chronic intestinal infection could induce autoimmune syndrome in mice and the specific antibody against the initiator might be lower or even disappear in the mature or late stage of the autoimmune syndrome.
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