ArticleOncogene2012
CD200-CD200R signaling suppresses anti-tumor responses independently of CD200 expression on the tumor.
Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03712488 (Differential Expression of CD200 in B-chronic Lymphoproliferative Disorders by Multicolour Flow Cytometry), which is not on this map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Differential Expression of CD200 in B-chronic Lymphoproliferative Disorders by Multicolour Flow Cytometry
Who cites it
40 citing papers in PubMed, 77 citations in OpenAlex.
- Plasma proteomics improves thrombosis prediction in patients with cancer and identifies targetable IL-17-driven endothelial activation.Science translational medicine · 2026Article
- Review
- CD200-CD200R as a myeloid immune checkpoint in solid tumors: mechanisms, context-dependent functions, and therapeutic opportunities.Frontiers in immunology · 2026Review
- CD200R blockade enhances anti-tumor immunity by unleashing NK and CD8Acta pharmacologica Sinica · 2025Article
- Targeting CD200 in Breast Cancer: Opportunities and Challenges in Immunotherapeutic Strategies.International journal of molecular sciences · 2024Review
- Necroptosis-based glioblastoma prognostic subtypes: implications for TME remodeling and therapy response.Annals of medicine · 2024Article
- The role of bone marrow microenvironment (BMM) cells in acute myeloid leukemia (AML) progression: immune checkpoints, metabolic checkpoints, and signaling pathways.Cell communication and signaling : CCS · 2023Review
- Combination CD200R/PD-1 blockade in a humanised mouse model.Immunotherapy advances · 2023Article
- Single-cell eQTL analysis of activated T cell subsets reveals activation and cell type-dependent effects of disease-risk variants.Science immunology · 2022Article
- The CD200-CD200R Axis Promotes Squamous Cell Carcinoma Metastasis via Regulation of Cathepsin K.Cancer research · 2021Article
- CD200 Immune-Checkpoint Peptide Elicits an Anti-glioma Response Through the DAP10 Signaling Pathway.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Article
- CD200 Blockade Modulates Tumor Immune Microenvironment but Fails to Show Efficacy in Inhibiting Tumor Growth in a Murine Model of Melanoma.Frontiers in cell and developmental biology · 2021Article
- The CD200/CD200R expression level and its mechanism of action in hematological malignancy patients.American journal of translational research · 2021Article
- Identification of a novel conserved signaling motif in CD200 receptor required for its inhibitory function.PloS one · 2021Article
- Targeting Neuroinflammation in Brain Cancer: Uncovering Mechanisms, Pharmacological Targets, and Neuropharmaceutical Developments.Frontiers in pharmacology · 2021Review
- CD200 is overexpressed in neuroblastoma and regulates tumor immune microenvironment.Cancer immunology, immunotherapy : CII · 2020Article
- CD200-CD200R Pathway in the Regulation of Tumor Immune Microenvironment and Immunotherapy.Advances in experimental medicine and biology · 2020Review
- CD200 and CD200R1 are differentially expressed and have differential prognostic roles in non-small cell lung cancer.Oncoimmunology · 2020Article
- NK Cell-Based Immune Checkpoint Inhibition.Frontiers in immunology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expression of CD200, the gene encoding the ligand for the inhibitory immune receptor CD200R, is an independent prognostic factor for various forms of leukemia predicting worse overall survival of the patients. The enhanced expression of CD200 on the tumors implies that anti-tumor responses can be enhanced by blockage of the CD200-CD200R interaction. Indeed, antibody-mediated blockade of the CD200-CD200R inhibitory axis is currently evaluated in clinical tests to boost immune responses against CD200-expressing tumors. Here, we show that mice lacking CD200, the exclusive ligand for CD200R, are resistant to chemical skin carcinogenesis. Importantly, CD200R controls tumor outgrowth independently of CD200 expression by the tumor cells themselves. Furthermore, Cd200(-/-) mice do not become tolerant to intranasally administered antigens, suggesting that tumor rejection is normally suppressed through CD200-induced immune tolerance. Decreased tumor outgrowth is accompanied by increased expression of the proinflammatory cytokines interleukin (IL)-1β and IL-6 by the lymph node (LN) dendritic cells. During carcinogenesis, skin-draining LNs of Cd200(-/-) mice contain increased numbers of IL-17-producing FoxP3(+) cells, which preferentially home to the tumors. Thus, the CD200-CD200R axis induces tolerance to external and tumor antigens and influences the T-regulatory/Th17 cell ratio. We demonstrate for the first time that the absence of CD200R signaling inhibits outgrowth of an endogenous tumor irrespective of CD200 expression by the tumor cells. This important paradigm shift leads to a much broader applicability of CD200-blockade in the treatment of tumors.
Indexed as
Identifiers
What OpenQuestion holds
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.