B-cell depletion reactivates B lymphopoiesis in the BM and rejuvenates the B lineage in aging
B-cell depletion reactivates B lymphopoiesis in the BM and rejuvenates the B lineage in aging
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DOI：
10.1182/blood-2010-09-307983
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发表时间：
2011-03-17
期刊：
影响因子：
20.3
通讯作者：
Melamed, Doron
中科院分区：
文献类型：
--
作者：
Keren, Zohar;Naor, Shulamit;Melamed, Doron
衰老与骨髓中B淋巴细胞生成的下降和外周中长寿B细胞的积累有关。这些变化降低了身体产生保护性抗体反应的能力。我们在这里表明，年龄相关的变化在B谱系介导的积累长寿B细胞。因此，耗尽老年小鼠中的B细胞后，多能原始祖细胞和普通淋巴祖细胞扩增，骨髓中B淋巴细胞生成的复苏，以及再生外周隔室的产生，其增强了动物对抗原刺激的免疫应答。总的来说，我们的研究结果表明，免疫衰老的B-谱系是不可逆的，并在老年小鼠的长寿B细胞的耗竭恢复B-谱系和增强免疫能力。（血。2011; 117（11）：3104-3112）
Aging is associated with a decline in B-lymphopoiesis in the bone marrow and accumulation of long-lived B cells in the periphery. These changes decrease the body's ability to mount protective antibody responses. We show here that age-related changes in the B lineage are mediated by the accumulating long-lived B cells. Thus, depletion of B cells in old mice was followed by expansion of multi-potent primitive progenitors and common lymphoid progenitors, a revival of B-lymphopoiesis in the bone marrow, and generation of a rejuvenated peripheral compartment that enhanced the animal's immune responsiveness to antigenic stimulation. Collectively, our results suggest that immunosenescence in the B-lineage is not irreversible and that depletion of the long-lived B cells in old mice rejuvenates the B-lineage and enhances immune competence. (Blood. 2011; 117(11): 3104-3112)