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Elevated TNFα induces hyperreactive platelets by reprogramming hematopoietic stem cells in mice

The inflammatory cytokine acts directly on stem cells rather than mature megakaryocytes, driving myeloid biasing and thromboinflammation through a persistent transcriptional program.

bioRxiv · Siner JI et al. · Paper published 29 Sep 2026

Paper

In mouse models, researchers investigated how chronic exposure to the inflammatory cytokine TNFα generates hyperreactive platelets. Using receptor labeling and single-cell RNA sequencing, the team found that megakaryocytes and their progenitors lack TNFα receptors. Instead, chronic TNFα expanded the hematopoietic stem and progenitor cell pool in bone marrow and extramedullary tissues. These expanded cells retained functional repopulation capacity. Activating TNFα receptor 1 signaling proved sufficient to cause platelet hyperreactivity even without progenitor cell expansion. Lineage-tracing experiments showed that chronic TNFα promoted megakaryocyte development through the canonical hematopoietic hierarchy rather than emergency hematopoiesis pathways. The exposure induced a distinct transcriptional program in stem cells and megakaryocytes that persisted through differentiation.

Why it matters

Because TNFα is a primary age-related cytokine, these findings explain how chronic inflammation can reprogram blood stem cells to promote thrombosis and thromboinflammation in aging.

Caveats

The findings are based entirely on mouse models and may not fully translate to humans. Additionally, this work is a preprint and has not yet undergone peer review.

Written from the paper’s abstract, and every claim checked against it before publishing. Read the paper for the full methods and data.

The paper

TNFα drives platelet hyperreactivity and thromboinflammation through regulation of hematopoietic stem and progenitor cells

Siner JI, Brakhane M, Platten K et al.

bioRxiv · 29 Sep 2026 · Preprint, not yet peer-reviewed

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