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December 8, 2025BloodOpen Access

LILRB4 drives proinflammatory cytokine secretion in multiple myeloma to promote the immune-cell dysfunction via the generation of myeloid-derived suppressive cells

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Authors

YWYijie Wang

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Overview

Findings reveal LILRB4 drives proinflammatory cytokine secretion in multiple myeloma, suggesting immune dysfunction by enhancing myeloid-derived suppressive cells.

Key Points

  • This research aims to elucidate how LILRB4 influences the immune microenvironment in multiple myeloma and contributes to immune cell dysfunction.
  • Analyzed the expression of LILRB4 in multiple myeloma patient samples via single-cell RNA sequencing.
  • Conducted in vivo and in vitro studies to assess the effects of LILRB4 on erythroid and myeloid cell interactions.
  • Evaluated the impact of CCL3 modulation on myeloma growth and immune cell populations.
  • LILRB4 overexpression was linked to increased myeloid-derived suppressor cells in multiple myeloma.
  • Deletion of CCL3 resulted in reduced myeloma cell growth and improved hemoglobin levels in blood.
  • Increased CD8⁺ T cell function and decreased regulatory T cell populations were observed with CCL3 deletion.

Cite This Study

Yijie Wang (2025) studied this question.

synapsesocial.com/papers/69362f3a4fa91c937236d3e2https://doi.org/10.1182/blood-2025-5695
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Also Consider

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

  1. 1LILRB4 represents a promising target for immunotherapy by dual targeting tumor cells and myeloid-derived suppressive cells in multiple myeloma2024 · 12 citations
  2. 2LILRB4 regulates multiple myeloma development through STAT3-PFKFB1 pathway2024 · 12 citations
  3. 3LILRB4 regulates multiple myeloma development through STAT3-PFKFB1 pathway2024
  4. 4The B2M–LILRB1 axis as a novel myeloid immune checkpoint and therapeutic target in multiple myeloma2025
  5. 5Abstract 364: Targeting LILRB1 to sensitize human myeloma to ferroptosis through disrupting cholesterol homeostasis2024