Murine experimental abortion by IL-2 administration is caused by activation of cytotoxic T lymphocytes and placental apoptosis.

Murine experimental abortion by IL-2 administration is caused by activation of cytotoxic T lymphocytes and placental apoptosis.
复制标题

IL-2 给药引起的小鼠实验性流产是由细胞毒性 T 淋巴细胞的激活和胎盘细胞凋亡引起的。

DOI:
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发表时间:
1996
期刊:
Journal of clinical & laboratory immunology
影响因子:
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通讯作者:
Kazuo Satoh
Kazuo Satoh
中科院分区:
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文献类型:
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作者:
H. Shiraishi;Satoshi Hayakawa;Kazuo Satoh

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目标 对怀孕小鼠施用IL-2引起的胎儿丢失被认为是由于同种免疫反应引起的人类习惯性流产的模型。为了评估该模型中的胎儿胎盘损伤,我们对胎盘中的细胞凋亡进行了组织化学检查。 方法 四只同种异体交配小鼠在交配后第 3 天、第 5 天 (7) 腹膜内注射 1000 IU 重组人 IL-2。我们通过 TUNEL 染色检查了胎盘中细胞凋亡的存在。我们还通过 RT-PCR 检查了 CTL 特异性颗粒酶 B/穿孔素 mRNA 的表达以及 TCR V β 受体片段的使用。 结果 1. 与对照小鼠相比,给予 IL-2 的同种异体怀孕小鼠显示绒毛滋养层细胞凋亡分数增加。从 IL-2 处理的胎盘中提取的 DNA 显示了梯状结构。 2.颗粒酶B mRNA表达增加,而穿孔素mRNA表达无变化。 3.我们观察到与未治疗的小鼠相比,IL-2治疗的小鼠蜕膜中TCR V beta基因片段的数量增加。 结论 我们认为母体CTL激活引起的胎盘细胞凋亡可能在胎儿同种异体移植物的排斥反应中发挥重要作用。
OBJECTIVE Fetal loss caused by IL-2 administration to pregnant mice is regarded as a model of human habitual abortion due to allo-immune reactions. To estimate feto-placental damages in this model, we examined apoptosis histochemically in the placenta. METHODS Four allogenic mated mice were administered intraperitoneally with 1000 IU of recombinant human IL-2 on days 3, 5 (7) after mating. We examined the presence of apoptosis in the placentae by TUNEL stain. We also examined expression of CTL specific granzyme B/perforin mRNA and usage of TCR V beta receptor segments by RT-PCR. RESULTS 1. Allogenic pregnant mice given IL-2 revealed increased apoptotic scores in villous trophoblasts compared with control mice. Extracted DNA from IL-2 treated placentae revealed ladder formations. 2. Expression of granzyme B mRNA was increased while expression of perforin mRNA was not changed. 3. We observed increased numbers of TCR V beta gene segments in the decidua from IL-2 treated mice compared with untreated mice. CONCLUSION We suggest that placental apoptosis caused by activation of maternal CTL may play important roles in the rejection of fetal allografts.