Innate immune pathways and inflammation in hematopoietic aging, clonal hematopoiesis, and MDS.
Innate immune pathways and inflammation in hematopoietic aging, clonal hematopoiesis, and MDS.
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造血老化、克隆性造血和MDS中的先天免疫途径和炎症。
DOI：
10.1084/jem.20201544
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发表时间：
2021-07-05
期刊：
影响因子：
--
通讯作者：
Starczynowski DT
中科院分区：
文献类型：
--
作者：
Trowbridge JJ;Starczynowski DT
先天免疫和炎症相关通路的失调与衰老、克隆造血和MDS相关的造血缺陷有关。我们回顾了该领域的现状和新兴概念，揭示了关键的生物学和新的治疗机会。随着老龄化人口的不断增长，迫切需要开发新的治疗策略来改善造血衰老疾病，包括克隆造血和骨髓增生异常综合征（MDS）。先天免疫和炎症相关途径的细胞内在失调以及全身性炎症与衰老、克隆造血和MDS相关的造血缺陷有关。在这里，我们回顾并讨论了先天免疫和炎症信号失调在白血病前期和mds衍生的造血细胞的竞争优势和克隆优势中的作用。我们还提出了新兴概念将如何进一步揭示关键的生物学和新的治疗机会。
Dysregulation of innate immune- and inflammatory-related pathways is implicated in hematopoietic defects associated with aging, clonal hematopoiesis, and MDS. We review the current state of this field and emerging concepts that reveal critical biology and novel therapeutic opportunities. With a growing aged population, there is an imminent need to develop new therapeutic strategies to ameliorate disorders of hematopoietic aging, including clonal hematopoiesis and myelodysplastic syndrome (MDS). Cell-intrinsic dysregulation of innate immune- and inflammatory-related pathways as well as systemic inflammation have been implicated in hematopoietic defects associated with aging, clonal hematopoiesis, and MDS. Here, we review and discuss the role of dysregulated innate immune and inflammatory signaling that contribute to the competitive advantage and clonal dominance of preleukemic and MDS-derived hematopoietic cells. We also propose how emerging concepts will further reveal critical biology and novel therapeutic opportunities.
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影响因子：
82.9
作者：
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通讯作者：
Steidl, Ulrich
影响因子：
30.8
作者：
Bonnefond, Amelie;Skrobek, Boris;Froguel, Philippe
通讯作者：
Froguel, Philippe
影响因子：
7.5
作者：
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DOI：
10.1200/edbk_239083
发表时间：
2019-01-01
期刊：
American Society of Clinical Oncology educational book. American Society of Clinical Oncology. Annual Meeting
影响因子：
--
作者：
DeZern, Amy E;Malcovati, Luca;Ebert, Benjamin L
通讯作者：
Ebert, Benjamin L
影响因子：
13.6
作者：
Akunuru S;Geiger H
通讯作者：
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