ArticleFrontiers in cell and developmental biology2025
CD248 induces PD-L1 expression on cancer-associated fibroblasts to promote NSCLC immune escape.
Article in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Cancer-associated fibroblasts in the lung cancer microenvironment from multi-dimensional mechanisms to therapeutic strategies.Frontiers in oncology · 2026Review
- Fibroblast transformation in the tumor microenvironment of lung adenocarcinoma: heterogeneity, regulation, and therapeutic targeting.Frontiers in immunology · 2026Review
- The Redox-Adhesion-Exosome (RAX) Hub in Cancer: Lipid Peroxidation-Driven EMT Plasticity and Ferroptosis Defense with HNE/MDA Signaling and Lipidomic Perspectives.Antioxidants (Basel, Switzerland) · 2025Review
- A bispecific antibody targeting PD-L1/TNFR2 increases tumor targeting and enhances antitumor efficacy in colorectal cancer.Journal for immunotherapy of cancer · 2025Article
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Authors and funding
20 authors.
Funding
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Abstract
Background: Tumor immune escape is a critical step in tumor progression. Cancer-associated fibroblasts (CAFs) in the tumor microenvironment (TME) express abundant PD-L1 and suppress the functions of CD8 Methods: Fibroblasts were isolated from tumor and normal lung tissues from patients. We detected the expression of CD248 and PD-L1 on CAFs. Then, the influence of CAFs inhibited the function of CD8 Results: Herein, we demonstrated that CD248 increased CAF PD-L1 levels, inhibiting CD8 Conclusion: Our findings demonstrate that CD248 activates FAK/Src/JNK/c-Jun, thereby inducing PD-L1 expression on CAFs, which promotes NSCLC immune escape.
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