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Plasma Cells Are Obligate Effectors of Enhanced Myelopoiesis in Aging Bone Marrow.
Immunity ( IF 25.5 ) Pub Date : 2019-07-11 , DOI: 10.1016/j.immuni.2019.06.006 Peter D Pioli 1 , David Casero 1 , Encarnacion Montecino-Rodriguez 1 , Sherie L Morrison 2 , Kenneth Dorshkind 1
Immunity ( IF 25.5 ) Pub Date : 2019-07-11 , DOI: 10.1016/j.immuni.2019.06.006 Peter D Pioli 1 , David Casero 1 , Encarnacion Montecino-Rodriguez 1 , Sherie L Morrison 2 , Kenneth Dorshkind 1
Affiliation
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Aging results in increased myelopoiesis, which is linked to the increased incidence of myeloid leukemias and production of myeloid-derived suppressor cells. Here, we examined the contribution of plasma cells (PCs) to age-related increases in myelopoiesis, as PCs exhibit immune regulatory function and sequester in bone marrow (BM). PC number was increased in old BM, and they exhibited high expression of genes encoding inflammatory cytokines and pathogen sensors. Antibody-mediated depletion of PCs from old mice reduced the number of myeloid-biased hematopoietic stem cells and mature myeloid cells to levels in young animals, but lymphopoiesis was not rejuvenated, indicating that redundant mechanisms inhibit that process. PCs also regulated the production of inflammatory factors from BM stromal cells, and disruption of the PC-stromal cell circuitry with inhibitors of the cytokines IL-1 and TNF-α attenuated myelopoiesis in old mice. Thus, the age-related increase in myelopoiesis is driven by an inflammatory network orchestrated by PCs.
中文翻译：
浆细胞是衰老的骨髓中增强的骨髓生成的专一性效应器。
衰老导致骨髓生成增加，这与髓样白血病的发生率增加和髓样抑制细胞的产生有关。在这里，我们检查了浆细胞（PCs）对骨髓生成与年龄相关的增加的贡献，因为PCs具有免疫调节功能和对骨髓（BM）的隔离。在老的BM中，PC数目增加，并且它们显示出编码炎性细胞因子和病原体传感器的基因的高表达。抗体介导的老龄小鼠PC耗竭可将幼年动物中偏向骨髓的造血干细胞和成熟髓细胞的数量降低到一定水平，但淋巴细胞生成并未恢复活力，表明多余的机制抑制了这一过程。PC还调节BM基质细胞产生炎症因子，细胞因子IL-1和TNF-α抑制剂可破坏PC基质细胞回路，并减缓老年小鼠的骨髓生成。因此，与年龄相关的骨髓生成增加是由PC精心策划的炎症网络驱动的。
更新日期：2019-07-12
中文翻译：
浆细胞是衰老的骨髓中增强的骨髓生成的专一性效应器。
衰老导致骨髓生成增加，这与髓样白血病的发生率增加和髓样抑制细胞的产生有关。在这里，我们检查了浆细胞（PCs）对骨髓生成与年龄相关的增加的贡献，因为PCs具有免疫调节功能和对骨髓（BM）的隔离。在老的BM中，PC数目增加，并且它们显示出编码炎性细胞因子和病原体传感器的基因的高表达。抗体介导的老龄小鼠PC耗竭可将幼年动物中偏向骨髓的造血干细胞和成熟髓细胞的数量降低到一定水平，但淋巴细胞生成并未恢复活力，表明多余的机制抑制了这一过程。PC还调节BM基质细胞产生炎症因子，细胞因子IL-1和TNF-α抑制剂可破坏PC基质细胞回路，并减缓老年小鼠的骨髓生成。因此，与年龄相关的骨髓生成增加是由PC精心策划的炎症网络驱动的。
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