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在Pten+/-小鼠中受损的Fas反应和自身免疫
A Di Cristofano1, P Kotsi, Y F Peng
1Department of Human Genetics-Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, Sloan-Kettering Institute, 1275 York Avenue, New York, NY 10021, USA.
Science (New York, N.Y.)
|September 25, 1999
概括
在PTEN基因的突变导致自身免疫性疾病通过损害Fas介导的亡. 抑制酸丁醇3-激酶 (PI3K) 恢复了Fas功能,使PI3K/Akt通路参与了这一过程.
科学领域:
- 免疫学 免疫学 免疫学
- 遗传学 是一个遗传学.
- 分子生物学分子生物学
背景情况:
- PTEN瘤抑制基因中的非活化突变与具有瘤易感性的人类疾病有关.
- PTEN编码了一种对细胞调节至关重要的酸酶.
- 与PTEN突变相关的自体主导性疾病尚未完全理解.
研究的目的:
- 研究PTEN在自身免疫性疾病中的作用.
- 阐明PTEN突变影响免疫细胞功能的机制.
- 探索PTEN,Fas介导的亡和自身免疫之间的联系.
主要方法:
- 产生和分析Pten异合体 (Pten+/-) 的小鼠.
- 在Pten+/-突变体中对自身免疫性疾病发展的评估.
- 评估Fas介导的亡和T淋巴细胞反应.
- 用酸丁醇 (PI) 3酶抑制剂对Pten+/-细胞的治疗.
主要成果:
- 在Pten+/-小鼠中,发生了一种致命的多克隆性自身免疫疾病.
- 在Pten+/-小鼠中,法斯介导的亡受损.
- 来自Pten+/-小鼠的T淋巴细胞表现出激活诱导的细胞死亡减少和增多.
- 酸丁醇 (PI) 3酶抑制剂恢复了Pten+/-细胞中的Fas反应.
结论:
- PTEN对于调解Fas反应和抑制自身免疫力至关重要.
- PI 3-激酶/Akt通路与PTEN在Fas介导的亡中的作用有关.
- 通过免疫细胞亡和增殖的失调,PTEN缺乏导致自身免疫病原发生.
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