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在Tet2缺乏宿主中,微生物信号驱动了白血病前骨髓扩散

Marlies Meisel^1,2, Reinhard Hinterleitner^1,2, Alain Pacis^3,4

¹Department of Medicine, University of Chicago, Chicago, IL, USA.

|May 18, 2018

概括

甲基细胞二氧化酶2 (TET2) 突变可能导致白血病. 在Tet2缺乏的小鼠中,肠壁功能障碍和微生物信号驱动了白血病前骨髓扩散,这表明了血液癌症的新治疗点.

科学领域:

血液学
免疫学
微生物学

背景情况:

在TET2 (tet甲基细胞二氧化酶2) 的体质突变驱动血液形成的恶性瘤.
TET2 缺陷增加了造血干细胞的自我更新,使发育偏向于骨髓系.
在Tet2缺陷模型中,白血病前骨髓扩散 (PMP) 是不完整的,这表明涉及外部因素.

研究的目的:

研究外在因素在 Tet2 缺陷小鼠中 PMP 的作用.
阐明肠道屏障功能,微生物信号和PMP之间的联系机制.
确定TET2突变的血液恶性瘤的潜在治疗策略.

主要方法:

使用不同程度的肠壁完整性的 Tet2 缺陷小鼠模型.
用细菌刺激和抗生素来评估PMP的发展和逆转.
分析了interleukin-6的产生和细菌转移.

主要成果:

由于小肠壁功能障碍导致的细菌转移和增加的互白素-6产量对于缺乏Tet2的小鼠的PMP至关重要.
通过破坏肠道屏障完整性或通过全身细菌刺激,可以在没有症状的Tet2缺乏的小鼠中诱导PMP.
抗生素治疗逆转了PMP,而没有细菌的Tet2缺乏的小鼠没有发展PMP,这突显了微生物信号的作用.

结论:

在Tet2缺乏的小鼠中需要微生物依赖性炎症.
肠壁功能障碍和随后的微生物转移是PMP的关键驱动因素.
这些发现为PMP透率的变化提供了机制基础,并为造血性恶性瘤提供了新的治疗途径.

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