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徐磊,潘永全,何明忠,高杰,陈飞兰.复发性实验性自身免疫性葡萄膜炎小鼠模型的诱导及其特点[J].陆军军医大学学报(原第三军医大学学报),2016,38(12):1432-1436.
Xu Lei,Pan Yongquan,He Mingzhong,Gao Jie,Chen Feilan.Induction and features of relapsing experimental autoimmune uveoretinitis in mice[J].J Amry Med Univ (J Third Mil Med Univ),2016,38(12):1432-1436.
徐磊,潘永全,何明忠,高杰,陈飞兰.复发性实验性自身免疫性葡萄膜炎小鼠模型的诱导及其特点[J].陆军军医大学学报(原第三军医大学学报),2016,38(12):1432-1436. DOI:
Xu Lei,Pan Yongquan,He Mingzhong,Gao Jie,Chen Feilan.Induction and features of relapsing experimental autoimmune uveoretinitis in mice[J].J Amry Med Univ (J Third Mil Med Univ),2016,38(12):1432-1436. DOI:
目的 诱导复发性实验性自身免疫性葡萄膜炎(experimental autoimmune uveoretinitis,EAU)小鼠模型,评价其发生过程及特点。 方法 完全弗氏佐剂(CFA)乳化的光感受器间维生素A类结合蛋白(IRBP)161-180肽段免疫B10.RⅢ小鼠作为诱导组(35只),用CFA-PBS免疫小鼠作为对照组(6只)。小鼠免疫后7、14、21、28、35 d裂隙灯显微镜和光学显微镜观察及评价眼部炎症发生、眼部表现和病理学变化;待炎症完全消失时,再次免疫小鼠,评价小鼠眼部炎症复发。 结果 诱导组首次免疫后7 d出现初发炎症,14 d炎症达高峰,随后炎症消退,至35 d完全消失。第35天进行再次免疫,36 d 出现复发炎症,42 d达炎症高峰,随后炎症消退,但至观察期第96天部分鼠(1/5)仍维持炎症。眼部表现为睫状充血、前房渗出、瞳孔受损。病理学表现为视网膜和脉络膜炎性细胞浸润,血管炎、肉芽肿性炎,光感受器细胞层破坏,视网膜下渗出。对照组未见明显炎症。 结论 建立的EAU呈现慢性复发性病程,其眼部表现和病理学特征与人类葡萄膜炎相似,可作为葡萄膜炎研究的新型动物模型。
Objective To induce and evaluate the onsets and features of relapsing experimental autoimmune uveoretinitis (EAU) in B10.RⅢ mice. Methods B10.RⅢ mice of the experimental group were immunized with interphotoreceptor retinoid-binding protein (IRBP) 161-180 peptides in complete Freund’s adjuvant (CFA)
while the mice of the control group were immunized with CFA-PBS. The clinical findings and histopathologic changes of both groups were observed at weekly intervals for 5 weeks after primary immunization. At the resolution of inflammation
the mice underwent secondary immunization with IRBP-CFA or CFA-PBS to evaluate the inflammation relapse. Results The primary inflammation signs were observed on the 7th day
rose to the peak on the 14th day
followed by gradual regression
and disappeared on the 35th day after primary immunization. The mice underwent secondary immunization on the 35th day after primary immunization. The relapsing inflammation signs were observed on the 36th day
and then rose to the climax on the 42nd day. The inflammation was alleviated on the 50th day
but about 1/5 of the mice still maintained inflammation signs on the 96th day after primary immunization. The main clinical findings in the mice were ciliary injection
corneal opacity
fibrinous exudates in the anterior chamber
and lesions of the pupil. The prominent histopathologic lesions included inflammatory cellular infiltration in the retina and choroid
retinal vasculitis and granuloma
disorganization and loss of photoreceptors
and subretinal exudates. Conclusion The relapsing EAU mouse model is characterized with chronic course and clinical and histopathologic findings similar to human uveitis
so it can be used as a suitable model for research of human uveitis.
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