ArticleJournal of translational medicine2022
Tumor-B-cell interactions promote isotype switching to an immunosuppressive IgG4 antibody response through upregulation of IL-10 in triple negative breast cancers.
Article in Journal of translational medicine, 2022. 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, 26 citations in OpenAlex.
- Humoral immunity in cancer.Signal transduction and targeted therapy · 2026Review
- Tumor-infiltrating B cells participate in shaping the immunosuppressive microenvironment in solid tumors.International journal of cancer · 2026Review
- Tumor microenvironment and key signaling pathways in breast cancer progression and therapy resistance: A review.Biomolecules & biomedicine · 2026Review
- Pertpy: an end-to-end framework for perturbation analysis.Nature methods · 2026Article
- Macrophages expressing chimeric cytokine receptors have an inflammatory phenotype and antitumoral activity upon IL-10 or TGFβ stimulation.Journal for immunotherapy of cancer · 2025Article
- The Role of Tumor Microenvironment in Triple-Negative Breast Cancer and Its Therapeutic Targeting.Cells · 2025Review
- Cytokine Networks in Triple-Negative Breast Cancer: Mechanisms, Therapeutic Targets, and Emerging Strategies.Biomedicines · 2025Review
- B cells enhance IL-1 beta driven invasiveness in triple negative breast cancer.Scientific reports · 2025Article
- Inflammation-associated drug resistance and tumor growth in TNBC.Frontiers in immunology · 2025Review
- Analysis of single-cell and spatial transcriptomics in TNBC cell-cell interactions.Frontiers in immunology · 2025Review
- Increased IgG4 expression within tertiary lymphoid structures of esophageal cancer and implications for prognosis.Frontiers in immunology · 2025Article
- Single-cell and spatial transcriptomics integration: new frontiers in tumor microenvironment and cellular communication.Frontiers in immunology · 2025Review
- B cells enhance IL-1 beta driven invasiveness in triple-negative breast cancer.Research square · 2024Article
- Both COVID-19 infection and vaccination induce high-affinity cross-clade responses to SARS-CoV-2 variants.iScience · 2022Article
- Review
- Prognostic analysis of cuproptosis-related gene in triple-negative breast cancer.Frontiers in immunology · 2022Article
- IL-10 revisited in systemic lupus erythematosus.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundTriple negative breast cancer (TNBC) is an aggressive breast cancer for which there is currently no targeted therapy. Tumor-infiltrating B-cells (TIB) have been observed in tumor tissues of TNBC patients, but their functional role is unclear. IgG4 is one of four antibody subclasses of IgG expressed and secreted by B cells. Unlike other IgG isotypes, IgG4 has an immunosuppressive function and is induced by Th2-type cytokines. In cancers such as melanoma, IgG4 has been linked with advanced disease and poor patient survival. Therefore, we sought to determine if IgG4 + B cells are present and determine the mechanisms driving isotype switching in TNBC.
methodsWe performed co-culture assays to examine expression of Th2 cytokines by TNBC cells with and without the presence of B cells. We also performed in vitro class switching experiments with peripheral B cells with and without co-culture with TNBC cells in the presence or absence of an IL-10 blocking antibody. We examined expression of CD20
resultsOur findings indicate that B cells interact with TNBC to drive chronic inflammatory responses through increased expression of inflammatory cytokines including the TH2 cytokines IL-4 and IL-10. In vitro class switching studies show that interactions between TNBC cell lines and B cells drive isotype switching to the IgG4 isotype in an IL-10 dependent manner. In patient tissues, expression of IgG4 correlates with CD20 and tumor expression of IL-10. Both IgG4 and tumor IL-10 are associated to shorter recurrence free survival (RFS) and overall survival (OS) in TNBC. In a multi-variant analysis, IL-10 was associated with poor outcomes indicating that tumor IL-10 may drive immune escape.
conclusionsThese findings indicate that interactions between TIB and TNBC results in activation of chronic inflammatory signals such as IL-10 and IL-4 that drive class switching to an IgG4 + subtype which may suppress antibody driven immune responses. The presence of IgG4 + B cells may serve as a biomarker for poor prognosis.
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