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December 8, 2025Blood

Disruption of IL-10 receptor signaling promotes hematopoietic stem cell exhaustion and clonal expansion of JAK2V617F mutant cells during inflammatory stress

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Authors

LWLucas WadleyJHJianhong C HeidmannHLHew Yeng Lai

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Overview

Disruption of IL-10 receptor signaling promotes HSC exhaustion and JAK2V617F clonal expansion in mice during inflammatory stress, suggesting implications for myeloproliferative neoplasms.

Key Points

  • Hematopoietic stem cells showed reduced quiescence following IL-10 receptor blockade, leading to exhaustion.
  • Prolonged cycling and metabolic pathway activation occurred in monocytes from mice treated with LPS plus IL-10R blockade.
  • Assessment using competitive transplantation demonstrated impaired regenerative function of HSCs from IL-10R-blocked mice.
  • Disruption of IL-10 receptor signaling may accelerate expansion of inflammation-resistant clones like JAK2V617F.

Cite This Study

Wadley et al. (2025) studied this question.

synapsesocial.com/papers/69362f514fa91c937236d976https://doi.org/10.1182/blood-2025-855
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Impaired IL-10 Receptor Signaling Leads to Inflammation Induced Exhaustion in Hematopoietic Stem Cells2025
  2. 2Interleukin-12 and TNFα signaling drives parallel evolution of independent leukemic clones in JAK2V617F mutant myeloproliferative neoplasms2025
  3. 3HMGA1 chromatin regulators drive transcriptional networks involved in megakaryocyte expansion, fibrosis, and sensitivity to interferon signaling in JAK2-V617F MPN2025
  4. 4Activation of integrin signaling up-regulates pro-inflammatory cytokines in JAK2-V617F positive hematopoietic cells2025 · 7 citations
  5. 5IL‑10 limits CLL progression by reprogramming T cell exhaustion and myeloid suppression2025