ArticleNPJ breast cancer2026
CD52 signaling via macrophage Siglec-G represents a therapeutic target for cancer immunotherapy.
Article in NPJ breast cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Pde1b controls cyclic nucleotide signaling in cDC1 and macrophages to regulate immune responses.EMBO reports · 2026Article
- Current therapeutic interventions to target cancer stem cells for metastasis.International journal of clinical oncology · 2026Review
- Spatial organization of the TNBC tumor microenvironment: multicellular niches, T-cell bottlenecks, and therapeutic opportunities.Journal of translational medicine · 2026Review
- CD24 as an innate immune checkpoint in solid tumors: biology, biomarker stratification, and therapeutic translation.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Triple-negative breast cancer (TNBC) remains a lethal malignancy with limited targeted therapies and high metastatic rates. Cancer cells evade macrophage clearance by overexpressing anti-phagocytic cell surface proteins, termed "don't eat me" signals. Blocking antibodies (e.g., anti-CD47) against these signals show therapeutic promise in multiple cancers, yet variable responses and limited durability of efficacy to such agents imply additional unknown "don't eat me" signals exist. Here, we detected positive CD52 expression in tumors from TNBC patients and demonstrated that CD52 on TNBC cells facilitates immune evasion by engaging the inhibitory receptor sialic acid-binding Ig-like lectin G (Siglec-G) on tumor-associated macrophages. Genetic ablation of either CD52 or Siglec-G, as well as antibody-mediated blockade of their interaction restored macrophage phagocytic activity both in vitro and in vivo. This consequently suppressed tumor progression, improved survival, and promoted an immunologically active tumor microenvironment in TNBC mouse models. Additionally, cotreatment with anti-CD52 sensitized tumor cells to PD-1 blockade therapy in the spontaneous MMTV-PyMT TNBC model. Our findings identify CD52 as a prominently expressed anti-phagocytic checkpoint in TNBC and reveal the therapeutic potential of dual PD-1/CD52 blockade as a novel immunotherapeutic strategy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.