ArticleMolecular therapy. Oncology2026
Depletion of IL-10 in CAR-NK cells augments reprogramming of the tumor microenvironment and ameliorates therapeutic efficacy.
Article in Molecular therapy. Oncology, 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
The ErbB2 (HER2)-specific CAR-engineered natural killer (NK) cell line NK-92/5.28.z is under investigation in a phase I clinical trial in glioblastoma patients. In preclinical studies, these cells demonstrated potent CAR-mediated cytotoxicity and stimulated endogenous antitumor immunity in immunocompetent animals. Pro-inflammatory cytokines can contribute to the CAR-NK cells' immunomodulatory activity, but this may be attenuated by immunosuppressive IL-10 that is also produced in substantial amounts by activated NK-92/5.28.z cells. To prevent IL-10 secretion, we modified the CAR-NK cells to express an intracellular anti-IL-10 antibody, which trapped IL-10 within the endoplasmic reticulum. This did not affect proliferation, phenotype, or cytotoxicity of the resulting NK-92/5.28.z/anti-IL10ER cells but strengthened their ability to mediate maturation of co-cultured dendritic cells and prevented M2-polarization of co-cultured macrophages induced by unmodified CAR-NK cells. In a syngeneic murine glioblastoma model, NK-92/5.28.z/anti-IL10ER cells exhibited enhanced antitumor activity and favored a pro-inflammatory tumor microenvironment characterized by reduced infiltration of IL-10-responsive immunosuppressive cell types. Our findings demonstrate that inhibiting IL-10 secretion improves the therapeutic potential of CAR-engineered NK-92 cells, suggesting this approach as a promising avenue for clinical translation.
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