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EZH2 mutations reprogram the immune response to yield a pre-malignant lymphoma niche [Single cell RNA-Seq (10X Genomics)]

ABSTRACT: EZH2 mutations reprogram the immune response to yield a pre-malignant lymphoma niche [Single cell RNA-Seq (10X Genomics)]

PROVIDER: PRJNA574272 | ENA |

REPOSITORIES: ENA

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EZH2 mutations reprogram the immune response to yield a pre-malignant lymphoma niche

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EZH2 mutations reprogram the immune response to yield a pre-malignant lymphoma niche [Single cell RNA-Seq (10X Genomics)]

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Project description:Follicular lymphomas (FLs) are slow-growing, indolent tumors containing extensive follicular dendritic cell (FDC) networks and recurrent EZH2 gain-of-function mutations. Paradoxically, FLs originate from highly proliferative germinal center (GC) B cells with proliferation strictly dependent on interactions with T follicular helper cells. Herein, we show that EZH2 mutations initiate FL by attenuating GC B cell requirement for T cell help and driving slow expansion of GC centrocytes that become enmeshed with and dependent on FDCs. By impairing T cell help, mutant EZH2 prevents induction of proliferative MYC programs. Thus, EZH2 mutation fosters malignant transformation by epigenetically reprograming B cells to form an aberrant immunological niche that reflects characteristic features of human FLs, explaining how indolent tumors arise from GC B cells.

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