ArticleiScience2023
Mathematical modeling identifies LAG3 and HAVCR2 as biomarkers of T cell exhaustion in melanoma.
Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Multiscale modeling of T cell exhaustion: A mathematical framework integrating continuous dynamics with spatial heterogeneity.PLoS computational biology · 2026Article
- Mathematical modeling of immune counter-regulation predicts efficacy of fractionated CD8Scientific reports · 2026Article
- The FGL1-LAG-3 axis attenuates melanoma-induced cachexia in mice.Cancer & metabolism · 2026Article
- Bulk and Single-Cell Transcriptomes Reveal Exhausted Signature in Prognosis of Hepatocellular Carcinoma.Genes · 2025Article
- Multomic analysis reveals the potential of LAG3 as a prognostic and immune biomarker and its validation in osteosarcoma.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cytotoxic T lymphocytes (CTLs) control tumors via lysis of antigen-presenting targets or through secretion of cytokines such as interferon-γ (IFNG), which inhibit tumor cell proliferation. Improved understanding of CTL interactions within solid tumors will aid the development of immunotherapeutic strategies against cancer. In this study, we take a systems biology approach to compare the importance of cytolytic versus IFNG-mediated cytostatic effects in a murine melanoma model (B16F10) and to dissect the contribution of immune checkpoints HAVCR2, LAG3, and PDCD1/CD274 to CTL exhaustion. We integrated multimodal data to inform an ordinary differential equation (ODE) model of CTL activities inside the tumor. Our model predicted that CTL cytotoxicity played only a minor role in tumor control relative to the cytostatic effects of IFNG. Furthermore, our analysis revealed that within B16F10 melanomas HAVCR2 and LAG3 better characterize the development of a dysfunctional CTL phenotype than does the PDCD1/CD274 axis.
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Registered trials
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