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Updated: Jan 26, 2026

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CD52 signaling via macrophage Siglec-G represents a therapeutic target for cancer immunotherapy

Xueting Qin1,2, Yixin Chang2, Yuanyuan Qiu3

  • 1School of Medicine, Nankai University, Tianjin, China.

NPJ Breast Cancer
|January 24, 2026
PubMed

Insights

Researchers identified CD52 as a novel "don't eat me" signal in triple-negative breast cancer (TNBC). Blocking CD52 restores macrophage clearance of cancer cells, offering a new immunotherapy strategy for TNBC.

Area of Science:

  • Immunology
  • Oncology
  • Cell Biology

Background:

  • Triple-negative breast cancer (TNBC) is aggressive with limited treatment options.
  • Cancer cells use "don't eat me" signals to evade immune cells like macrophages.
  • Existing therapies targeting these signals show variable efficacy, suggesting unknown mechanisms exist.

Purpose of the Study:

  • To identify novel anti-phagocytic checkpoints in TNBC.
  • To investigate the role of CD52 in TNBC immune evasion.
  • To evaluate the therapeutic potential of targeting the CD52-Siglec-G axis.

Main Methods:

  • Detected CD52 expression in TNBC patient tumors.
  • Utilized genetic ablation and antibody blockade of CD52 and Siglec-G.
  • Assessed macrophage phagocytic activity in vitro and in vivo.
  • Evaluated tumor progression, survival, and immune microenvironment in TNBC mouse models.
  • Tested combination therapy with anti-CD52 and PD-1 blockade.

Main Results:

  • CD52 is expressed on TNBC cells and engages Siglec-G on macrophages, inhibiting phagocytosis.
  • Blocking CD52 or Siglec-G restored macrophage phagocytosis, suppressed tumor growth, and improved survival in TNBC models.
  • Targeting CD52 promoted an immunologically active tumor microenvironment.
  • Combined anti-CD52 and PD-1 blockade enhanced therapeutic efficacy in a spontaneous TNBC model.

Conclusions:

  • CD52 is a key anti-phagocytic checkpoint in TNBC, contributing to immune evasion.
  • Targeting the CD52-Siglec-G pathway offers a promising therapeutic strategy for TNBC.
  • Dual PD-1/CD52 blockade represents a novel and potentially effective immunotherapy for TNBC.

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