ArticleImmunology2021
B2M gene expression shapes the immune landscape of lung adenocarcinoma and determines the response to immunotherapy.
Article in Immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 66 citations in OpenAlex.
- Tumor suppressor genotype influences the extent and mode of immunosurveillance in lung cancer.Nature communications · 2026Article
- Redundant and distinct mechanisms suppress innate immune activation during SARS-CoV-2 infection.PLoS biology · 2026Article
- Decoding the tumor microenvironment remodeling orchestrated by CLEC3B+ inflammatory cancer-associated fibroblasts in lung adenocarcinoma immunotherapy: elucidation from pan-cancer spatially single-cell transcriptomics landscape.Journal of translational medicine · 2026Article
- Tumor PD-L1 induces β2m ubiquitylation and degradation for cancer cell immune evasion.Cell research · 2026Article
- Defects in antigen processing and presentation: mechanisms, immune evasion and implications for cancer vaccine development.Nature reviews. Immunology · 2026Review
- Exploring a mutation-based signature to predict the benefits of immune checkpoint inhibitors in oncogene-addicted subsets of non-small cell lung cancer: a retrospective study.Respiratory research · 2025Article
- Integrated Transcriptomic Analysis of S100A8/A9 as a Key Biomarker and Therapeutic Target in Sepsis Pathogenesis and AI Drug Repurposing.International journal of molecular sciences · 2025Article
- RTP4 Suppresses Colorectal Cancer Progression via MHC-I-Mediated CD8Journal of cellular and molecular medicine · 2025Article
- Inhibiting KRAS with CD47 and immune checkpoint overcomes intrinsic resistance to combined KRAS and immune checkpoint inhibitor therapy.Cell reports. Medicine · 2025Article
- Identification of malignant cells in single-cell transcriptomics data.Communications biology · 2025Review
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- Tumor Immunosenescence Driven by Chronic Inflammation: Mechanisms, Microenvironment Remodeling and Therapeutic Strategies.Aging and disease · 2025Review
- An in vivo "turning model" reveals new RanBP9 interactions in lung macrophages.Cell death discovery · 2025Article
- Society for Immunotherapy of Cancer (SITC) consensus statement on essential biomarkers for immunotherapy clinical protocols.Journal for immunotherapy of cancer · 2025Article
- STModule: identifying tissue modules to uncover spatial components and characteristics of transcriptomic landscapes.Genome medicine · 2025Article
- Article
- The role of B2M in cancer immunotherapy resistance: function, resistance mechanism, and reversal strategies.Frontiers in immunology · 2025Review
- Overcoming resistance to immune checkpoint inhibitor in non-small cell lung cancer: the promise of combination therapy.Frontiers in immunology · 2025Review
- Glycolytic reprogramming of resident alveolar macrophages contributes to reduced SOCS3 secretion in non-small cell lung cancer.Frontiers in immunology · 2025Article
- Utilizing Nanoparticles to Overcome Anti-PD-1/PD-L1 Immunotherapy Resistance in Non-Small Cell Lung cancer: A Potential Strategy.International journal of nanomedicine · 2025Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Loss of the B2M gene is associated with tumour immune escape and resistance to immunotherapy. However, genetic alterations of the B2M gene are rare. We performed an integrative analysis of the mutational and transcriptional profiles of large cohorts of non-small-cell lung cancer (NSCLC) patients and found that epigenetic downregulation of B2M is common. B2M-low tumours exhibit a suppressive immune microenvironment characterized by reduced infiltration of immune cells of various lineages; in B2M-high tumours, more T and natural killer cells are present, but their activities are constrained by immune checkpoint molecules, indicating the diverse mechanisms of immune evasion. High levels of B2M mRNA, but not PD-L1, are correlated with an enhanced response to PD-1-based immunotherapy, suggesting its value for immunotherapy response prediction in solid tumours. Notably, a high tumour mutation burden (TMB) is associated with low B2M expression, which may explain the poor predictive value of the TMB in some situations. In syngeneic mouse models, genetic ablation of B2M in tumour cells causes resistance to PD-1-based immunotherapy, and B2M knockdown also diminishes the therapeutic efficacy. Moreover, forced expression of B2M in tumour models improves the response to immunotherapy, suggesting that B2M levels have significant impacts on treatment outcomes. Finally, we provide insight into the roles of transcription factors and KRAS mutations in B2M expression and the anticancer immune response. In conclusion, genetic and epigenetic regulation of B2M fundamentally shapes the NSCLC immune microenvironment and may determine the response to checkpoint blockade-based immunotherapy.
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