Language
English
Publication Date
11-1-2024
Journal
Nature Cell Biology
DOI
10.1038/s41556-024-01508-6
PMID
39266726
PMCID
PMC12228142
PubMedCentral® Posted Date
11-1-2025
PubMedCentral® Full Text Version
Author MSS
Abstract
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.
Keywords
Humans, Female, Myeloid Cells, B-Lymphocytes, Immune Tolerance, Cell Communication, Triple Negative Breast Neoplasms, Myelopoiesis, Animals, Neutrophils, T-Lymphocytes, Mice, Tumor Microenvironment, Middle Aged
Published Open-Access
yes
Recommended Citation
Hao, Xiaoxin; Shen, Yichao; Liu, Jun; et al., "Solid Tumour-Induced Systemic Immunosuppression Involves Dichotomous Myeloid-B Cell Interactions" (2024). Faculty and Staff Publications. 4901.
https://digitalcommons.library.tmc.edu/baylor_docs/4901
Included in
Health Services Research Commons, Medical Cell Biology Commons, Medical Molecular Biology Commons, Medical Specialties Commons, Microbiology Commons