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An IL-1β-driven neutrophil–stromal cell axis fosters a BAFF-rich protumor microenvironment in individuals with multiple myeloma
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An IL-1β-driven neutrophil–stromal cell axis fosters a BAFF-rich protumor microenvironment in individuals with multiple myeloma
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Journal Article
An IL-1β-driven neutrophil–stromal cell axis fosters a BAFF-rich protumor microenvironment in individuals with multiple myeloma
2024
Overview
Human bone marrow permanently harbors high numbers of neutrophils, and a tumor-supportive bias of these cells could significantly impact bone marrow-confined malignancies. In individuals with multiple myeloma, the bone marrow is characterized by inflammatory stromal cells with the potential to influence neutrophils. We investigated myeloma-associated alterations in human marrow neutrophils and the impact of stromal inflammation on neutrophil function. Mature neutrophils in myeloma marrow are activated and tumor supportive and transcribe increased levels of
IL1B
and myeloma cell survival factor
TNFSF13B
(BAFF). Interactions with inflammatory stromal cells induce neutrophil activation, including BAFF secretion, in a STAT3-dependent manner, and once activated, neutrophils gain the ability to reciprocally induce stromal activation. After first-line myeloid-depleting antimyeloma treatment, human bone marrow retains residual stromal inflammation, and newly formed neutrophils are reactivated. Combined, we identify a neutrophil–stromal cell feed-forward loop driving tumor-supportive inflammation that persists after treatment and warrants novel strategies to target both stromal and immune microenvironments in multiple myeloma.
Cupedo and colleagues show that neutrophils promote a tumor-supportive microenvironment via a self-amplifying interaction between neutrophils and bone marrow stromal cells. This scenario creates a promyeloma niche that is difficult to treat despite targeted therapies directed at the myeloma cells.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
