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Cancer coopts differentiation of B-cell precursors into macrophages

ABSTRACT: Cancer coopts differentiation of B-cell precursors into macrophages

PROVIDER: PRJNA747688 | ENA |

REPOSITORIES: ENA

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Cancer coopts differentiation of B-cell precursors into macrophages [mouse]

Project description:Cancer coopts differentiation of B-cell precursors into macrophages [mouse]

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Cancer coopts differentiation of B-cell precursors into macrophages [human]

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Cancer coopts differentiation of B-cell precursors into macrophages [mouse]

Project description:We recently reported that some cancers induce accumulation of bone marrow (BM) B-cell precursors in the spleen to convert them into metastasis-promoting, immunosuppressive B cells. Here, using various murine tumor models and samples from humans with breast and ovarian cancers, we provide evidence that cancer cells also coopt differentiation of the extranodal B-cell precursors to generate macrophages (termed B-MF). We link the trans-differentiation to a small subset of CSF1R+ Pax5Lo cells within BM pro-/pre-B and immature B cells and cancer-secreted M-CSF that downregulates Pax5 via CSF1R signaling. Thus, cancer generates tumor-associated macrophages (TAM) from B-cell precursors besides their primary source, monocytes. Based on their differences from monocyte-derived TAM, such as a superb ability to induce FoxP3+ Tregs, suppress proliferation of T cells and more efficiently phagocytize apoptotic cells, we propose that cancer generates B-MF to mediate cancer escape.

2021-09-20 | GSE180283 | GEO

Cancer coopts differentiation of B-cell precursors into macrophages [human]

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B-cell derived macrophage in mouse and human breast cancer macrophage

Project description:Cancer actively uses B cells to promote its progression and metastasis. For example, it causes accumulation of bone marrow (BM) B-cell precursors in spleen to convert into immunosuppressive Breg cells. Here, we provide evidence that cancer also coopts differentiation BM CSF1R+ Pax5Lo B-cell precursors to generate macrophages (termed B-MF cells). To do this, cancer uses CSF1 to trigger Csf1r signaling and downregulate PAX5 in B-cell precursors by activating FOXO1. Although tumor-associated macrophages (TAMs) are primarily derived from BM monocytes, our data suggest that some of them may have B-cell origin. Unlike monocyte-derived TAMs, B-MF exhibit a higher M2 polarization, more efficiently phagocytize apoptotic cells, induce FoxP3+ Tregs and suppress T cells activity. We propose that the cancer-B-MF axis is a novel immune escape pathway, thus a therapeutic target.

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Project description:Transcriptional profiling of a directed differentiation time course converting human embryonic stem cells (hES) into immature pancreatic beta cell precursors.

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