脾脏
下调和上调
免疫系统
生物
免疫学
T细胞
细胞生物学
细胞毒性T细胞
免疫
细胞
血红素加氧酶
血红素
细胞生长
间质细胞
内分泌学
内科学
新陈代谢
表型
毒性
细胞免疫
淋巴结
癌症研究
T淋巴细胞
缺铁
免疫耐受
化学
作者
David Ezuz,Heba Ombashe,Lana Watad,akmaral Rakhymzhanova,Surya Prakash Pandey,Orna Atar,Esther G. Meyron‐Holtz,Noga Ron‐Harel
出处
期刊:Nature Aging
日期:2025-10-17
卷期号:5 (11): 2247-2262
被引量:3
标识
DOI:10.1038/s43587-025-00981-4
摘要
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.
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