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首页> 外文期刊>Nature immunology >Impaired thymic development in mouse embryos deficient in apoptotic DNA degradation.
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Impaired thymic development in mouse embryos deficient in apoptotic DNA degradation.

机译：缺乏凋亡DNA降解的小鼠胚胎胸腺发育受损。

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摘要

Apoptosis is often accompanied by the degradation of chromosomal DNA. Caspase-activated DNase (CAD) is an endonuclease that is activated in dying cells, whereas DNase II is present in the lysosomes of macrophages. Here, we show that CAD(-/-) thymocytes did not undergo apoptotic DNA degradation. But, when apoptotic cells were phagocytosed by macrophages, their DNA was degraded by DNase II. The thymus of DNase II(-/-)CAD(-/-) embryos contained many foci carrying undigested DNA and the cellularity was severely reduced due to a block in T cell development. The interferon-beta gene was strongly up-regulated in the thymus of DNase II(-/-)CAD(-/-) embryos, suggesting that when the DNA of apoptotic cells is left undigested, it can activate innate immunity leading to defects in thymic development.
机译：凋亡通常伴随着染色体DNA的降解。半胱天冬酶激活的DNase（CAD）是一种在死亡细胞中被激活的核酸内切酶，而DNase II存在于巨噬细胞的溶酶体中。在这里，我们显示CAD（-/-）胸腺细胞未经历凋亡性DNA降解。但是，当凋亡细胞被巨噬细胞吞噬时，它们的DNA被DNase II降解。脱氧核糖核酸酶II（-/-）CAD（-/-）胚胎的胸腺含有许多携带未消化的DNA的病灶，并且由于T细胞发育受阻而严重降低了细胞性。干扰素-β基因在DNase II（-/-）CAD（-/-）胚胎的胸腺中强烈上调，表明当凋亡细胞的DNA不被消化时，它可以激活先天免疫，导致缺陷。胸腺发育。

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