ArticleNature cancer2025
PILRα on tumor cells interacts with the T cell surface protein CD99 to suppress antitumor immunity.
Article in Nature cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed.
- Leveraging multimodal cancer immunotherapy to amplify the efficacy of oncolytic viruses.Experimental hematology & oncology · 2026Review
- VSIG4 suppresses antitumor T cell immunity via the SLC3A2-dependent metabolic-ionic checkpoint.Journal for immunotherapy of cancer · 2026Article
- Recent advances in the construction of humanized animal models and applications in translational medicine.Animal models and experimental medicine · 2026Review
- Immune Checkpoint Inhibitors and Immunomodulators for Cancer Immunotherapy: Insights Into Resistance and Therapeutic Strategies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- HOXD13-mediated immune crosstalk between cancer cells and tumor-associated macrophages drives colorectal cancer progression.Journal for immunotherapy of cancer · 2026Article
- Innate immune signaling-driven myeloid remodeling in cancer: inflammatory amplification, immune suppression, and therapeutic targeting.Frontiers in immunology · 2026Review
- Research on the Mechanism of "Cold Tumor" Formation and Immunotherapy for Its Transformation into "Hot Tumor".Oncology research · 2026Review
- Integrating bulk RNA-seq and ScRNA-seq to identify manganese metabolism-related subtypes and immunoregulatory mechanisms in liver hepatocellular carcinoma.Open life sciences · 2026Article
- CD99 is a potential diagnostic and immunological biomarker in pan-cancer.Discover oncology · 2025Article
- Breakthroughs in immune checkpoint therapy: overcoming NSCLC immune checkpoint therapy resistance with novel techniques.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Immune checkpoint blockade using anti-programmed cell death protein 1/programmed cell death 1 ligand 1 antibody effectively targets the tumor-T cell interaction in cancer treatment, yet the overall response rate of less than 30% necessitates the identification of additional immune checkpoints modulating T cell function. Here, we identified the tumor cell-expressed paired immunoglobulin-like type 2 receptor alpha (PILRα) as an immune suppressor targeting T cells using high-throughput screening. PILRα inhibits T cell activation, proliferation and effector function by targeting CD99, a T cell surface antigen, suppressing ZAP70/NFAT/IL-2/JAK/STAT signaling. A cluster of O-glycosylated serine and threonine residues within the stalk region is critical for PILRα-CD99 interactions. Blocking these interactions with a stalk-targeting anti-PILRα antibody enhances T cell antitumor immunity and suppresses tumor growth. When combined with programmed cell death protein 1 antibody, anti-PILRα antibody shows synergistic tumor suppression. Notably, PILRα is highly expressed in several human cancers and predicts poor prognosis. These findings unveil PILRα as an immune checkpoint with therapeutic potential for clinical cancer immunotherapy.
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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.