老年脾脏血红素和铁毒性通过铁剥夺损害T细胞免疫。

IF 19.4 Q1 CELL BIOLOGY
David Ezuz, Heba Ombashe, Lana Watad, Akmaral Rakhymzhanova, Satyarth Pandey, Orna Atar, Esther G Meyron-Holtz, Noga Ron-Harel
{"title":"老年脾脏血红素和铁毒性通过铁剥夺损害T细胞免疫。","authors":"David Ezuz, Heba Ombashe, Lana Watad, Akmaral Rakhymzhanova, Satyarth Pandey, Orna Atar, Esther G Meyron-Holtz, Noga Ron-Harel","doi":"10.1038/s43587-025-00981-4","DOIUrl":null,"url":null,"abstract":"<p><p>Mechanisms of T cell aging involve cell-intrinsic alterations and interactions with immune and stromal cells. Here we found that splenic T cells exhibit greater functional decline than lymph node T cells within the same aged mouse, prompting investigation into how the aged spleen contributes to T cell aging. Proteomic analysis revealed increased expression of heme detoxification in aged spleen-derived lymphocytes. Exposure to the heme- and iron-rich aged splenic microenvironment induced aging phenotypes in young T cells, including reduced proliferation and CD39 upregulation. T cells survived this hostile niche by maintaining a low labile iron pool, at least in part, via IRP2 downregulation to resist ferroptosis but failed to induce sufficient iron uptake for activation. Iron supplementation enhanced antigen-specific T cell responses in aged mice. This study identifies the aged spleen as a source of hemolytic signals that systemically impair T cell function, underscoring a trade-off between T cell survival and function and implicating iron metabolism in immune aging.</p>","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":" ","pages":""},"PeriodicalIF":19.4000,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Heme and iron toxicity in the aged spleen impairs T cell immunity through iron deprivation.\",\"authors\":\"David Ezuz, Heba Ombashe, Lana Watad, Akmaral Rakhymzhanova, Satyarth Pandey, Orna Atar, Esther G Meyron-Holtz, Noga Ron-Harel\",\"doi\":\"10.1038/s43587-025-00981-4\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Mechanisms of T cell aging involve cell-intrinsic alterations and interactions with immune and stromal cells. Here we found that splenic T cells exhibit greater functional decline than lymph node T cells within the same aged mouse, prompting investigation into how the aged spleen contributes to T cell aging. Proteomic analysis revealed increased expression of heme detoxification in aged spleen-derived lymphocytes. Exposure to the heme- and iron-rich aged splenic microenvironment induced aging phenotypes in young T cells, including reduced proliferation and CD39 upregulation. T cells survived this hostile niche by maintaining a low labile iron pool, at least in part, via IRP2 downregulation to resist ferroptosis but failed to induce sufficient iron uptake for activation. Iron supplementation enhanced antigen-specific T cell responses in aged mice. This study identifies the aged spleen as a source of hemolytic signals that systemically impair T cell function, underscoring a trade-off between T cell survival and function and implicating iron metabolism in immune aging.</p>\",\"PeriodicalId\":94150,\"journal\":{\"name\":\"Nature aging\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":19.4000,\"publicationDate\":\"2025-10-17\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nature aging\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1038/s43587-025-00981-4\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nature aging","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1038/s43587-025-00981-4","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

T细胞衰老的机制包括细胞内在的改变以及与免疫细胞和基质细胞的相互作用。在这里,我们发现在同一年老小鼠中,脾脏T细胞比淋巴结T细胞表现出更大的功能衰退,这促使人们对衰老的脾脏如何促进T细胞衰老进行研究。蛋白质组学分析显示老龄脾源性淋巴细胞血红素解毒表达增加。暴露于富含血红素和铁的衰老脾微环境会诱导年轻T细胞的衰老表型,包括增殖减少和CD39上调。T细胞通过维持一个低不稳定的铁池存活下来,至少部分是通过IRP2下调来抵抗铁凋亡,但未能诱导足够的铁摄取来激活。补充铁可增强老年小鼠的抗原特异性T细胞反应。这项研究发现,衰老的脾脏是溶血信号的来源,系统性地损害T细胞功能,强调T细胞生存和功能之间的权衡,并暗示铁代谢与免疫衰老有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Heme and iron toxicity in the aged spleen impairs T cell immunity through iron deprivation.

Mechanisms of T cell aging involve cell-intrinsic alterations and interactions with immune and stromal cells. Here we found that splenic T cells exhibit greater functional decline than lymph node T cells within the same aged mouse, prompting investigation into how the aged spleen contributes to T cell aging. Proteomic analysis revealed increased expression of heme detoxification in aged spleen-derived lymphocytes. Exposure to the heme- and iron-rich aged splenic microenvironment induced aging phenotypes in young T cells, including reduced proliferation and CD39 upregulation. T cells survived this hostile niche by maintaining a low labile iron pool, at least in part, via IRP2 downregulation to resist ferroptosis but failed to induce sufficient iron uptake for activation. Iron supplementation enhanced antigen-specific T cell responses in aged mice. This study identifies the aged spleen as a source of hemolytic signals that systemically impair T cell function, underscoring a trade-off between T cell survival and function and implicating iron metabolism in immune aging.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
CiteScore
14.70
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信