ArticleThe Journal of clinical investigation2015
Immunosurveillance and therapy of multiple myeloma are CD226 dependent.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 84 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
84 citing papers in PubMed, 139 citations in OpenAlex.
- Diagnosis, risk stratification and management of smouldering multiple myeloma.Nature reviews. Clinical oncology · 2026Review
- Identification of Bone Marrow and Peripheral Blood Plasma Extracellular Vesicle Protein Biomarker Signatures for Multiple Myeloma Diagnosis and Staging.International journal of nanomedicine · 2026Article
- Molecular and immunological determinants of long-term survival in multiple myeloma.Blood advances · 2025Review
- The predictive effect of the CD155-TIGIT immune checkpoint axis complex on neoadjuvant chemotherapy efficacy in triple-negative breast cancer: A preliminary study.Cancer biomarkers : section A of Disease markers · 2025Article
- The Immune Regulatory Functions of CD226 and Its Implications in Immune-Mediated Diseases.Biomolecules · 2025Review
- Modeling the Bone Marrow Niche in Multiple Myeloma: From 2D Cultures to 3D Systems.International journal of molecular sciences · 2025Review
- Polyfunctional CD8Molecular oncology · 2025Article
- The multifaceted role of SMAD4 in immune cell function.Biochemistry and biophysics reports · 2025Review
- One-carbon metabolism is distinct metabolic signature for proliferative intermediate exhausted T cells of ICB-resistant cancer patients.Cell death discovery · 2025Article
- Depletion of myeloid-derived suppressor cells sensitizes murine multiple myeloma to PD-1 checkpoint inhibitors.Journal for immunotherapy of cancer · 2025Article
- T Cells Dysfunction in Multiple Myeloma.ImmunoTargets and therapy · 2025Review
- Interferon gamma-mediated prevention of tumor progression in a mouse model of multiple myeloma.HemaSphere · 2024Article
- Tumor-induced natural killer cell dysfunction is a rapid and reversible process uncoupled from the expression of immune checkpoints.Science advances · 2024Article
- HLA class I NK-epitopes and KIR diversities in patients with multiple myeloma.Immunogenetics · 2024Article
- Next-Generation Therapies for Multiple Myeloma.Annual review of cancer biology · 2024Article
- Diet-induced obesity reduces bone marrow T and B cells and promotes tumor progression in a transplantable Vk*MYC model of multiple myeloma.Scientific reports · 2024Article
- The role of exhausted natural killer cells in the immunopathogenesis and treatment of leukemia.Cell communication and signaling : CCS · 2024Review
- Immune microenvironment in papillary thyroid carcinoma: roles of immune cells and checkpoints in disease progression and therapeutic implications.Frontiers in immunology · 2024Review
- IL6Myc mouse is an immunocompetent model for the development of aggressive multiple myeloma.Haematologica · 2023Article
- Increased innate immune activation induces protective RSV-specific lung-resident memory T cells in neonatal mice.Mucosal immunology · 2023Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
- Correction · 2015-07-01Concerns/Issues about Authorship/Affiliation · Error in Image · Error in Text ·
- Erratum issuedImmunosurveillance and therapy of multiple myeloma are CD226 dependent.2015 · Chesi, Martha [corrected to Chesi, Marta]
Authors and funding
15 authors at 7 institutions in 5 countries.
Funding
Abstract
Multiple myeloma (MM) is an age-dependent hematological malignancy. Evaluation of immune interactions that drive MM relies on in vitro experiments that do not reflect the complex cellular stroma involved in MM pathogenesis. Here we used Vk*MYC transgenic mice, which spontaneously develop MM, and demonstrated that the immune system plays a critical role in the control of MM progression and the response to treatment. We monitored Vk*MYC mice that had been crossed with Cd226 mutant mice over a period of 3 years and found that CD226 limits spontaneous MM development. The CD226-dependent anti-myeloma immune response against transplanted Vk*MYC MM cells was mediated both by NK and CD8+ T cells through perforin and IFN-γ pathways. Moreover, CD226 expression was required for optimal antimyeloma efficacy of cyclophosphamide (CTX) and bortezomib (Btz), which are both standardly used to manage MM in patients. Activation of costimulatory receptor CD137 with mAb (4-1BB) exerted strong antimyeloma activity, while inhibition of coinhibitory receptors PD-1 and CTLA-4 had no effect. Taken together, the results of this study provide in vivo evidence that CD226 is important for MM immunosurveillance and indicate that specific immune components should be targeted for optimal MM treatment efficacy. As progressive immunosuppression associates with MM development, strategies aimed to increase immune functions may have important therapeutic implications in MM.
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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.