Precursor B acute lymphoblastic leukemia (BCP-ALL), the most common childhood malignancy, arises from an expansion of malignant B cell precursors in the bone marrow. Epidemiological studies suggest that infections or immune responses to infections may promote such an expansion and thus BCP-ALL development. Nevertheless, a specific pathogen responsible for this process has not been identified. BCP-ALL cells critically depend on interactions with the bone marrow microenvironment. The bone marrow is also home to memory T helper (Th) cells that have previously expanded during an immune response in the periphery. In secondary lymphoid organs, Th cells can interact with malignant cells of mature B cell origin, while such interactions between Th cells and malignant immature B cell in the bone marrow have not been described yet. Nevertheless, literature supports a model where Th cells—expanded during an infection in early childhood—migrate to the bone marrow and support BCP-ALL cells as they support normal B cells. Further research is required to mechanistically confirm this model and to elucidate the interaction pathways between leukemia cells and cells of the tumor microenvironment. As benefit, targeting these interactions could be included in current treatment regimens to increase therapeutic efficiency and to reduce relapses.

中文翻译：

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小儿前体 B 急性淋巴细胞白血病：T 辅助细胞是传染性病因学理论中的缺失环节吗？

前体 B 急性淋巴细胞白血病 (BCP-ALL) 是最常见的儿童恶性肿瘤，起源于骨髓中恶性 B 细胞前体的扩增。流行病学研究表明，感染或对感染的免疫反应可能会促进这种扩张，从而促进 BCP-ALL 的发展。然而，尚未确定负责该过程的特定病原体。BCP-ALL 细胞严重依赖与骨髓微环境的相互作用。骨髓也是记忆 T 辅助 (Th) 细胞的家园，这些 T 细胞先前在外周免疫反应期间已经扩增。在次级淋巴器官中，Th细胞可以与成熟B细胞来源的恶性细胞相互作用，而骨髓中Th细胞与恶性未成熟B细胞之间的这种相互作用尚未被描述。尽管如此，文献支持一种模型，其中 Th 细胞（在儿童早期感染期间扩增）迁移到骨髓并支持 BCP-ALL 细胞，因为它们支持正常 B 细胞。需要进一步的研究来从机制上确认该模型并阐明白血病细胞与肿瘤微环境细胞之间的相互作用途径。作为好处，针对这些相互作用可以包括在当前的治疗方案中，以提高治疗效率并减少复发。