PDF(Pubmed)
Abstract：
The occurrence of clonal hematopoiesis of indeterminate potential (CHIP), in which advantageous somatic mutations result in the clonal expansion of blood cells, increases with age, as do an increased risk of mortality and detrimental outcomes associated with CHIP. However, the role of CHIP in susceptibility to pulmonary infections, which also increase with age, is unclear. In this issue of the JCI, Quin and colleagues explored the role of CHIP in bacterial pneumonia. Using characterization of immune cells from human donors and mice lacking tet methylcytosine dioxygenase 2 (Tet2), the authors mechanistically link myeloid immune cell dysfunction to CHIP-mediated risk of bacterial pneumonia. The findings suggest that CHIP drives inflammaging and immune senescence, and provide Tet2 status in older adults as a potential prognostic tool for informing treatment options related to immune modulation.
摘要：
不确定潜能（CHIP）的克隆造血的发生，其中有利的体细胞突变导致血细胞的克隆扩增，随着年龄的增长，与CHIP相关的死亡和有害结局风险增加。然而,CHIP在肺部感染易感性中的作用，随着年龄的增长，不清楚。在本期JCI中，Quin及其同事探讨了CHIP在细菌性肺炎中的作用。使用来自人类供体和缺乏tet甲基胞嘧啶双加氧酶2（Tet2）的小鼠的免疫细胞的表征，作者将髓系免疫细胞功能障碍与CHIP介导的细菌性肺炎风险进行了机械联系.研究结果表明，CHIP驱动炎症和免疫衰老，并在老年人中提供Tet2状态作为一种潜在的预后工具，用于告知与免疫调节相关的治疗方案。
