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June 13, 2026Journal for ImmunoTherapy of CancerOpen Access

Tumor-derived HMGB2 induces M2-like macrophage polarization via TRIM65-mediated NLRP3 degradation to promote DLBCL progression

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Authors

SHSanxiu HeYLYing LiuYTYifeng Tang

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Overview

Randomized trial investigates HMGB2's role in macrophage polarization in DLBCL, suggesting new therapeutic strategies.

Key Points

  • This research aims to unveil the role of HMGB2 in promoting M2-like macrophage polarization and its implications for DLBCL progression.
  • Analyzed HMGB2 expression in DLBCL using public databases and validated through quantitative reverse transcription-PCR and western blot.
  • Constructed HMGB2 knockdown models in vivo and in vitro, establishing macrophage-DLBCL co-culture systems to study macrophage polarization.
  • Utilized transcriptome sequencing and protease protection assays to uncover molecular mechanisms of HMGB2 action.
  • HMGB2 overexpression correlates with poor prognosis in DLBCL patients.
  • Knockdown of HMGB2 suppressed tumor progression in vivo by altering the tumor microenvironment.
  • Exosomal HMGB2 promotes TRIM65-mediated degradation of NLRP3 in macrophages, leading to M2-like polarization and impaired phagocytosis.

Cite This Study

He et al. (2026) studied this question.

synapsesocial.com/papers/6a2cf551faef96ed7f057658https://doi.org/10.1136/jitc-2026-015018
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