ArticleNature communications2026
Extracellular vesicle proteins monitor and interfere with CLDN18.2-targeted CAR-T cell and antibody therapies against gastrointestinal cancers.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Claudin 18.2 (CLDN18.2)-targeted CAR-T cell and antibody therapies show promise against gastrointestinal cancers, but biomarkers predictive of long-term benefit and therapeutic sensitization strategies are needed. Here we show that proteins carried by circulating extracellular vesicles (EVs) can reflect and influence the efficacy of CLDN18.2-targeted therapies. By profiling serial plasma samples of patients from the CT041-CG4006 trial (CLDN18.2- CAR-T-therapy) or the GLOW trial (Zolbetuximab), we identified EV-associated CLDN18.2, PD1 and PD-L2 as therapeutic markers and integrated them into a signature (CPP-score) for better predictive robustness. Mechanistically, specific EV-proteins exhaust CAR-T cells, neutralize CLDN18.2-targeted-antibodies, activate immunosuppressive IL-6-expressing cancer-associated fibroblasts, and alter the TH1/TH2 balance, thereby reshaping the tumor microenvironment and interfere with CLDN18.2-targeted therapies. Strategies including combining anti-PD1 antibody or CAF inhibitor, CLDN18.2-CAR-T plus CLDN18.2-antibody, and depleting plasma EVs, can sensitize CLDN18.2-CAR-T/antibody by countermeasuring EV-proteins' therapeutic interferences. Collectively, our work provides potential options to monitor and improve CLDN18.2-targeted therapies in clinical practice.
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