Age-associated loss of lamin-B leads to systemic inflammation and gut hyperplasia.
Age-associated loss of lamin-B leads to systemic inflammation and gut hyperplasia.
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DOI：
10.1016/j.cell.2014.10.028
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发表时间：
2014-11-06
期刊：
影响因子：
64.5
通讯作者：
Zheng Y
中科院分区：
文献类型：
--
作者：
Chen H;Zheng X;Zheng Y
Aging of immune organs, termed as immunosenescence, is suspected to promote systemic inflammation and age-associated disease. The cause of immunosenescence and how it promotes disease, however, has remained unexplored. We report that the Drosophila fat body, a major immune organ, undergoes immunosenescence and mounts strong systemic inflammation that leads to de-regulation of immune deficiency (IMD) signaling in the midgut of old animals. Inflamed old fat bodies secrete circulating peptidoglycan recognition proteins that repress IMD activity in the midgut, thereby promoting gut hyperplasia. Further, fat body immunosenecence is caused by age-associated lamin-B reduction specifically in fat body cells, which then contributes to heterochromatin loss and de-repression of genes involved in immune responses. As lamin-associated heterochromatin domains are enriched for genes involved in immune response in both Drosophila and mammalian cells, our findings may provide insights into the cause and consequence of immunosenescence during aging.
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