ArticleOncotarget2017
MM-BMSCs induce naïve CD4+ T lymphocytes dysfunction through fibroblast activation protein α.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Bone Marrow Adipocytes in Multiple Myeloma: Emerging Immunometabolic Interactions and Implications for Immunotherapy.Cancers · 2026Review
- Review
- Fibrillar extracellular matrix produced by pericyte-like cells facilitates glioma cell dissemination.Brain pathology (Zurich, Switzerland) · 2024Article
- From basic research to clinical application: targeting fibroblast activation protein for cancer diagnosis and treatment.Cellular oncology (Dordrecht, Netherlands) · 2024Review
- The immune system in multiple myeloma and precursor states: Lessons and implications for immunotherapy and interception.American journal of hematology · 2023Review
- Beta-endoproteolysis of the cellular prion protein by dipeptidyl peptidase-4 and fibroblast activation protein.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Targeting TGF-β signaling in the multiple myeloma microenvironment: Steering CARs and T cells in the right direction.Frontiers in cell and developmental biology · 2022Review
- Armored BCMA CAR T Cells Eliminate Multiple Myeloma and Are Resistant to the Suppressive Effects of TGF-β.Frontiers in immunology · 2022Article
- Pro-tumorigenic roles of fibroblast activation protein in cancer: back to the basics.Oncogene · 2018Review
- LncRNA Expression in CD4+ T Cells in Neurosyphilis Patients.Frontiers in cellular and infection microbiology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe tumor microenvironment plays a major role in multiple myelomas (MM). MM-BMSCs (bone marrow mesenchymal stromal cells) can support tumor growth and immune surveillance escape. On the other hand, fibroblast activation protein α, expressed by cancer stroma cells including BMSCs, has been shown to potentiate epithelial cancers growth and immune suppression.
resultsMM-BMSC inhibited proliferation of T cells ( MATERIALS AND
methodsThe expression of FAPα was analyzed by western blot and RT-PCR. The proliferation and senescence of CD4+ T cells was examined by cck-8 and β-gal staining, and Treg/Th17, CD28 expression was analyzed by FCM. The FAPα and PI3K pathway was analyzed by western blot and their relationship with T cell function was detected by FCM and RT-PCR. The level of IL-10, IL-17 and TGF-β was detected by ELISA.
conclusionsMM-BMSCs inhibit T-cell proliferation and drive Th17 differentiation through FAPα/TGF-β axis, leading to the progression of myeloma. FAPα-induced T-cell senescence is mediated by the PI3K signaling pathway.
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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.