Background Experimental autoimmune uveoretinitis(EAU)is proved to be an organ-specific,T lymphocyte-mediated autoimmune and self-limited disease.Research showed that CD4+CD25+T cell may play important regulation on the course of events,but its mechanism is pending for further study. Objective Present study was to investigate the potential role of CD4+CD25+T cell in the pathogenesis of EAU. Methods Retinal Santigen(S-Ag)was isolated from bovine retinas according tO the procedure as Caspi's previously describe.0.1 ml Santigen(50μg)emulsified with complete Freund'S adjuvant was injected on footpad of 24 inbred adult female Lewis rats aged six to eight-week-old to induce EAU,and 4 normal Lewis rats were as normal control group.Slim-lamp examination was performed to observe the ocular manifestation.Retinal section was prepared in 7,12,15,21 days aher injection for the pathological examination.The pathological grading was on the lnoki'S method.The retinas,inguinal nodes and spleens of rats were obtained in 7,12,15,21 days after injection and the cellular suspension was prepared.Expression of CD4+CD25+T cells on cellular suspension was assayed using flow eytometry.This study complied with the Standard of Association for Research in Vision and Ophthalmology. ResuRs The obvious inflammatory response of the anterior segment was found in S-Ag injected eyes from 7 days through 21 days.The most serious inflammation was found in 12-15 days under the slim-lamp.The hemotoxylin and eosin staining showed the higher pathological grading from 12 to 15 days after injection,showing significant difference in comparison with 7 days and 14 days(P=0.000).In EAU model rats,expressions of CD4+CD25+T cells was significantly increased in retinas, inguinal nodes and spleens in 15 days after injection,showing evidently differences in comparison with control rats(P=0.000). Conclusion The expression level of CD4+CD25+T cells in inflammatory tissue is associated with the inflammation procedure in EAU model rats.This study indicates that CD4+CD25+T cells may play a role in the development of EAU.%背景 实验性自身免疫性葡萄膜视网膜炎(EAU)已被证明是一种由T淋巴细胞介导的器官特异性自限性疾病.研究表明CD4+CD25+T细胞可能参与了EAU的调控,但其作用机制尚有待研究.目的 探讨EAU中CD4+CD25+T细胞的表达变化.方法 按照Caspi的方法提纯牛视网膜S抗原,与弗氏完全佐剂混合后,于24只Lewis大鼠右后足底部注射0.1 ml制作EAU模型,4只未处理大鼠作为正常对照组.免疫后每日用裂隙灯显微镜观察大鼠眼部变化.造模后7、12、15、21 d处死动物,取大鼠视网膜、引流淋巴结、脾脏,对大鼠眼组织切片进行苏木精-伊红染色并进行病理评分.对各时间点收集的大鼠视网膜、引流淋巴结、脾脏分别制备单细胞悬液,流式细胞仪检测各时间点3种组织中CD4+CD25+T细胞的表达情况.结果 造模7 d后大鼠睫状充血,虹膜血管扩张;15 d后炎症达高峰,前房大量炎性渗出;21 d后炎症消退.眼部病理评分结果与临床所见一致,造模15 d组病理评分与其他各组比较差异均有统计学意义(P=0.000).正常对照组大鼠脾脏和淋巴结中有2.0%CD4+T细胞表达CD25,造模组CD4+CD25+T细胞表达增加,并在EAU高峰期达最高,EAU消退期轻微下降,与正常对照组比较差异有统计学意义(P=0.000).结论 CD4+CD25+T细胞在EAU动物模型炎症组织中表达的动态变化与炎症反应有关,提示CD4+CD25+T细胞参与EAU的发生发展和消退过程.
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