实体瘤会诱导涉及骨髓细胞和 T 细胞的全身免疫抑制。 B 细胞相关机制的研究相对较少。在这里，我们发现了肿瘤诱导的 B 细胞异常的两种不同模式（TiBA；TiBA-1 和 TiBA-2），两者都与骨髓中的异常骨髓生成​​有关。 TiBA-1可能是前祖B细胞和骨髓祖细胞之间的生态位竞争的结果，导致下游B细胞的整体减少。 TiBA-2 的特点是独特的早期 B 细胞群的系统积累，由与过量中性粒细胞的相互作用驱动。重要的是，TiBA-2 相关的早期 B 细胞促进了耗竭样 T 细胞的全身积累。来自三阴性乳腺癌患者外周血的骨髓细胞和 B 细胞概括了 TiBA 亚型，并且独特的 TiBA 谱与对标准护理免疫治疗的病理完全反应相关。这项研究强调了肿瘤引起的全身变化的患者间多样性，并强调需要针对不同 B 细胞和骨髓细胞异常进行量身定制的治疗。© 2024。作者，获得 Springer Nature Limited 的独家许可。

Solid tumours induce systemic immunosuppression that involves myeloid and T cells. B cell-related mechanisms remain relatively understudied. Here we discover two distinct patterns of tumour-induced B cell abnormality (TiBA; TiBA-1 and TiBA-2), both associated with abnormal myelopoiesis in the bone marrow. TiBA-1 probably results from the niche competition between pre-progenitor-B cells and myeloid progenitors, leading to a global reduction in downstream B cells. TiBA-2 is characterized by systemic accumulation of a unique early B cell population, driven by interaction with excessive neutrophils. Importantly, TiBA-2-associated early B cells foster the systemic accumulation of exhaustion-like T cells. Myeloid and B cells from the peripheral blood of patients with triple-negative breast cancer recapitulate the TiBA subtypes, and the distinct TiBA profile correlates with pathologic complete responses to standard-of-care immunotherapy. This study underscores the inter-patient diversity of tumour-induced systemic changes and emphasizes the need for treatments tailored to different B and myeloid cell abnormalities.© 2024. The Author(s), under exclusive licence to Springer Nature Limited.