DHEAS enhances germinal center responses in old mice.

DHEAS enhances germinal center responses in old mice.
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DHEAS 增强老年小鼠的生发中心反应。

DOI:
10.1007/978-1-4615-2492-2_38
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发表时间:
1994
影响因子:
--
通讯作者:
Szakal,AK
Szakal,AK
中科院分区:
医学4区
文献类型:
--
作者:
Caffrey,RE;Kapasi,ZF;Haley,ST;Tew,JG;Szakal,AK

文献摘要

被引文献

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抗原(Ag)转运导致保银fdc网的形成。研究表明,在年龄较大(23个月)的小鼠淋巴结中,银转运存在缺陷,只有一小部分预期的银转运位点发育。发育的Ag转运位点形成球状结构的萎缩不连续通路。抗原刺激后第1-3天,Ag转运缺陷对应于fdc保留网状细胞数量的类似缺陷。发育的滤泡树突状细胞在超微结构上萎缩,保留少量银,不产生糖原体。在最近的研究中,我们研究了FDC保银网缺陷的老年小鼠生发中心发育能力。利用生发中心B细胞的花生凝集素(PNA)与PNA-辣根过氧化物酶(HRP)偶联物的组织化学结合特征,通过图像分析监测生发中心的发育。结果显示生发中心发育有明显的年龄相关性。有趣的是,fdc网状细胞数量与生发中心数量的比例保持在1:1,与年轻免疫小鼠的情况相似。这些比率支持免疫小鼠生发中心发育需要保银FDC的概念,这一观察结果与最近的体外数据完全一致。因此,老年小鼠缺乏产生生发中心的能力反映了与抗原运输和FDC发育相关的年龄相关缺陷。
Antigen (Ag) transport leads to the formation of the Ag retaining FDC-reticulum.1Studies have demonstrated that in old (23 month) mouse lymph nodes, Ag transport is defective and only a small fraction of the expected Ag transport sites develops.2The Ag transport sites that develop, form atrophic discontinuous pathways of globular structures. The Ag transport deficit corresponds to a similar deficit in the number of FDC-retaining reticula by day 1–3 after antigenic challenge. Follicular dendritic cells that develop are ultrastructurally atrophic, retain little Ag, and produce no iccosomes. In recent studies, we examined the capacity for germinal center development in old mice with a deficit of FDC Ag-retaining reticula. Germinal center development was monitored by image analysis utilizing the peanut agglutinin (PNA) binding feature of germinal center B cells histochem-ically with PNA-horseradish peroxidase (HRP) conjugates.3The results showed a marked age-related depression of germinal center development. Interestingly, the ratio of FDC-reticula to germinal center numbers remained 1:1, similarly to that shown for young immune mice.3These ratios support the concept that germinal center development in immune mice requires Ag-retaining FDC, an observation in complete agreement with the more recentin vitrodata.4Thus the lack of capacity of old mice to produce germinal centers reflects age-related defects associated with antigen transport and FDC development.