ArticleJCI insight2017
C3d regulates immune checkpoint blockade and enhances antitumor immunity.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- The role of the complement system in gastrointestinal-related diseases.Frontiers in immunology · 2026Review
- Adoptive cell therapy against tumor immune evasion: mechanisms, innovations, and future directions.Frontiers in oncology · 2025Review
- Complement C3d enables cell-mediated immunity capable of distinguishing spontaneously transformed from nontransformed cells.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Somatic Cell Fusion in Host Defense and Adaptation.Results and problems in cell differentiation · 2024Article
- Complement factor H: a novel innate immune checkpoint in cancer immunotherapy.Frontiers in cell and developmental biology · 2024Review
- C3-dependent effector functions of complement.Immunological reviews · 2023Review
- Review
- Targeting the Complement Pathway in Malignant Glioma Microenvironments.Frontiers in cell and developmental biology · 2021Review
- Complement controls the immune synapse and tumors control complement.Journal for immunotherapy of cancer · 2020Article
- DHX37 Impacts Prognosis of Hepatocellular Carcinoma and Lung Adenocarcinoma through Immune Infiltration.Journal of immunology research · 2020Article
- Neutrophil: A New Player in Metastatic Cancers.Frontiers in immunology · 2020Review
- Non-canonical B cell functions in transplantation.Human immunology · 2019Review
- Article
- Complementing the Cancer-Immunity Cycle.Frontiers in immunology · 2019Review
- Article
- B Cells in Transplantation of Rat, Mouse, and Man.Transplantation · 2018Article
- The mutable vaccine for mutable viruses.Immunotherapy · 2017Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Despite expression of immunogenic polypeptides, tumors escape immune surveillance by engaging T cell checkpoint regulators and expanding Tregs, among other mechanisms. What orchestrates these controls is unknown. We report that free C3d, a fragment of the third component of complement, inside tumor cells - or associated with irradiated tumor cells and unattached to antigen - recruits, accelerates, and amplifies antitumor T cell responses, allowing immunity to reverse or even to prevent tumor growth. C3d enhances antitumor immunity independently of B cells, NK cells, or antibodies, but it does so by increasing tumor infiltrating CD8+ lymphocytes, by depleting Tregs, and by suppressing expression of programmed cell death protein 1 (PD-1) by T cells. These properties of C3d appear specific for the tumor and dependent on complement receptor 2, and they incur no obvious systemic toxicity. The heretofore unrecognized properties of free C3d suggest that protein might determine the effectiveness of immune surveillance and that increasing availability of the protein might prove advantageous in the treatment or prevention of cancer and premalignant conditions.
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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.