ArticleScience advances2022
The immune checkpoint B7-H3 (CD276) regulates adipocyte progenitor metabolism and obesity development.
Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The trial behind it
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Who cites it
22 citing papers in PubMed, 22 citations in OpenAlex.
- Immune checkpoints and immunoregulation in metabolic diseases and cancers: pathological mechanisms and therapeutic potential.Signal transduction and targeted therapy · 2026Review
- B7-H3 promotes skin photodamage through ITGA2-NRF2-TFAM-mediated mitochondrial oxidative stress.Communications biology · 2026Article
- B7-H3 interaction with cMet enhances lipolysis to drive malignant progression of glioma via pSTAT3-ATGL axis.Journal of translational medicine · 2026Article
- B7-H3 in the tumor microenvironment: Implications for CAR T cell therapy in pediatric solid tumors.Cancer metastasis reviews · 2025Review
- The B7-H3 (CD276) pathway: emerging biology and clinical therapeutics.Trends in pharmacological sciences · 2025Review
- B7-H3/CD276: Novel Immune Checkpoint and Jack of All Trades.ImmunoTargets and therapy · 2025Review
- Research progress of B7-H3 in malignant tumors.Frontiers in immunology · 2025Review
- Revealing the mechanisms and therapeutic potential of immune checkpoint proteins across diverse protein families.Frontiers in immunology · 2025Review
- Sex-Specific Effects of THRβ Signaling on Metabolic Responses to High Fat Diet in Mice.Endocrinology · 2024Article
- Immunoregulation in cancer-associated cachexia.Journal of advanced research · 2024Review
- B7-H3 at the crossroads between tumor plasticity and colorectal cancer progression: a potential target for therapeutic intervention.Cancer metastasis reviews · 2024Review
- B7-H3 promotes proliferation and migration of lung cancer cells by modulating PI3K/AKT pathway via ENO1 activity.Translational cancer research · 2024Article
- A promising target for breast cancer: B7-H3.BMC cancer · 2024Review
- B7-H3 in glioblastoma and beyond: significance and therapeutic strategies.Frontiers in immunology · 2024Review
- B7H3 increases ferroptosis resistance by inhibiting cholesterol metabolism in colorectal cancer.Cancer science · 2023Article
- Therapeutic Targets of Monoclonal Antibodies Used in the Treatment of Cancer: Current and Emerging.Biomedicines · 2023Review
- Recent advancements in the B7/CD28 immune checkpoint families: new biology and clinical therapeutic strategies.Cellular & molecular immunology · 2023Review
- Article
- B7H3 Role in Reshaping Immunosuppressive Landscape in MSI and MSS Colorectal Cancer Tumours.Cancers · 2023Article
- New frontiers in immune checkpoint B7-H3 (CD276) research and drug development.Molecular cancer · 2023Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
The immune checkpoint B7-H3 (CD276) is a member of the B7 family that has been studied in the tumor microenvironment and immunotherapy, but its potential role in metabolism remains largely unknown. Here, we show that B7-H3 is highly expressed in mouse and human adipose tissue at steady state, with the highest levels in adipocyte progenitor cells. B7-H3 is rapidly down-regulated upon the initiation of adipocyte differentiation. Combined RNA sequencing and metabolic studies reveal that B7-H3 stimulates glycolytic and mitochondrial activity of adipocyte progenitors. Loss of B7-H3 in progenitors results in impaired oxidative metabolism program and increased lipid accumulation in derived adipocytes. Consistent with these observations, mice knocked out for B7-H3 develop spontaneous obesity, metabolic dysfunction, and adipose tissue inflammation. Our results reveal an unexpected metabolic role for B7-H3 in adipose tissue and open potential new avenues for the treatment of metabolic diseases by targeting the B7-H3 pathway.
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.