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2型呼肠孤病毒感染小鼠的胸腺萎缩:免疫抑制及胸腺激素的作用。reo-2引起的胸腺萎缩

Thymic atrophy in type 2 reovirus infected mice: immunosuppression and effects of thymic hormone. Thymic atrophy caused by reo-2.

作者信息

Onodera T, Taniguchi T, Tsuda T, Yoshihara K, Shimizu S, Sato M, Awaya A, Hayashi T

机构信息

National Institute of Animal Health, Ibaraki, Japan.

出版信息

Thymus. 1991 Sep;18(2):95-109.

PMID:1656552
Abstract

Suckling mice infected with reovirus type 2 showed a thymic atrophy followed by a marked suppression of the antibody, production to SRBC (a T cell dependent antigen) and bacterial LPS, when measured by the splenic PFC assay. The PFCs produced were sometimes less than 1% of uninfected control animals. Histologically the thymus was usually smaller than normal, and atrophy of the cortex and increased number of Hassal's bodies were observed. Number of nucleated cells in the thymus of infected mice showed 90% decrease as compared to uninfected mice. The spleen, although larger in size, showed depletion of lymphocytes from the thymus-dependent and follicular areas. No viral replication was detected in lymphatic organs using virological methods. Virus-infected mice transferred with the splenocytes or thymocytes from age-matched uninfected mice restored the antibody production against SRBC to normal levels. Thymocytes were more efficient than splenocytes in enhancing the antibody production in virus-infected mice. Injection of several different kinds of immunopotentiating agents enhanced the antibody production to SRBC, although LPS exacerbated the unresponsiveness. Thymic hormones such as FTS and TP5 enhanced antibody production to SRBC and LPS more efficiently than MDP. Flow cytometric analysis showed that percentage of CD4+ single positive cells was slightly increased in virus-infected mice treated with FTS, while there was no difference in the phenotypic distributions of thymocyte subpopulations among virus-infected mice, FTS-untreated and FTS-treated normal mice.

摘要

感染2型呼肠孤病毒的乳鼠出现胸腺萎缩,随后通过脾空斑形成细胞(PFC)试验检测发现,其对绵羊红细胞(一种T细胞依赖性抗原)和细菌脂多糖的抗体产生受到显著抑制。产生的PFC有时不到未感染对照动物的1%。组织学检查显示,胸腺通常比正常小,观察到皮质萎缩和哈氏小体数量增加。与未感染小鼠相比,感染小鼠胸腺中有核细胞数量减少了90%。脾脏虽然体积较大,但胸腺依赖区和滤泡区的淋巴细胞减少。使用病毒学方法在淋巴器官中未检测到病毒复制。将年龄匹配的未感染小鼠的脾细胞或胸腺细胞转移到病毒感染小鼠体内,可使针对绵羊红细胞的抗体产生恢复到正常水平。在增强病毒感染小鼠的抗体产生方面,胸腺细胞比脾细胞更有效。注射几种不同的免疫增强剂可增强针对绵羊红细胞的抗体产生,尽管脂多糖会加剧无反应性。胸腺激素如FTS和TP5比MDP更有效地增强了针对绵羊红细胞和脂多糖的抗体产生。流式细胞术分析显示,用FTS处理的病毒感染小鼠中CD4 + 单阳性细胞的百分比略有增加,而在病毒感染小鼠、未用FTS处理的正常小鼠和用FTS处理的正常小鼠之间,胸腺细胞亚群的表型分布没有差异。

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