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Sublethal Total Body Irradiation Causes Long-Term Deficits in Thymus Function by Reducing Lymphoid Progenitors

淋巴细胞生成 胸腺退化 造血 生物 骨髓 全身照射 祖细胞 胸腺细胞 内卷(密宗) 干细胞 免疫学 男科 癌症研究 T细胞 免疫系统 医学 细胞生物学 遗传学 化疗 神经科学 意识 环磷酰胺
作者
Shiyun Xiao,Ivo Shterev,Wen Zhang,Lauren Young,Jae-Hung Shieh,Malcolm A.S. Moore,Marcel R.M. van den Brink,Gregory D. Sempowski,Nancy R. Manley
出处
期刊:Journal of Immunology [The American Association of Immunologists]
卷期号:199 (8): 2701-2712 被引量:31
标识
DOI:10.4049/jimmunol.1600934
摘要

Abstract Total body irradiation (TBI) damages hematopoietic cells in the bone marrow and thymus; however, the long-term effects of irradiation with aging remain unclear. In this study, we found that the impact of radiation on thymopoiesis in mice varied by sex and dose but, overall, thymopoiesis remained suppressed for ≥12 mo after a single exposure. Male and female mice showed a long-term dose-dependent reduction in thymic cKit+ lymphoid progenitors that was maintained throughout life. Damage to hematopoietic stem cells (HSCs) in the bone marrow was dose dependent, with as little as 0.5 Gy causing a significant long-term reduction. In addition, the potential for T lineage commitment was radiation sensitive with aging. Overall, the impact of irradiation on the hematopoietic lineage was more severe in females. In contrast, the rate of decline in thymic epithelial cell numbers with age was radiation-sensitive only in males, and other characteristics including Ccl25 transcription were unaffected. Taken together, these data suggest that long-term suppression of thymopoiesis after sublethal irradiation was primarily due to fewer progenitors in the BM combined with reduced potential for T lineage commitment. A single irradiation dose also caused synchronization of thymopoiesis, with a periodic thymocyte differentiation profile persisting for at least 12 mo postirradiation. This study suggests that the number and capability of HSCs for T cell production can be dramatically and permanently damaged after a single relatively low TBI dose, accelerating aging-associated thymic involution. Our findings may impact evaluation and therapeutic intervention of human TBI events.

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