ArticleJournal for immunotherapy of cancer2026
Chemotherapy induces an IL1β-dependent neutrophil recruitment and activation that promote chemoresistance in metastatic ovarian cancer.
Article in Journal for immunotherapy of cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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21 authors.
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Abstract
backgroundHigh-grade serous carcinoma (HGSC) of the ovary acquires chemoresistance through diverse cancer cell-intrinsic and cell-extrinsic mechanisms, culminating in treatment-refractory intraperitoneal metastasis. Previous work suggests that chemotherapy induces immunological changes in the tumor microenvironment (TME). However, experimental evidence for how such chemotherapy-induced TME remodeling modulates the response to ongoing chemotherapy remains poorly documented in HGSC.
methodsWe analyzed paired pre-chemotherapy and post-chemotherapy HGSC bulk transcriptomic and single-cell RNA sequencing (scRNA-seq) datasets to identify chemotherapy-induced tumor-extrinsic factors and their cellular sources in the TME. To test causality, we used chemoresistant, homologous recombination-proficient murine metastatic HGSC models with deficiencies in the interleukin 1 beta (IL1β) pathway (IL1β-interleukin 1 receptor type 1 (IL1R1) axis). Flow cytometry and scRNA-seq of omental tumors were used to define cellular interactions. Contributions of neutrophils and neutrophil extracellular traps (NETs) were assessed by antibody-mediated depletion and immunofluorescence. Direct effects of IL1β and NETs on cancer cell chemosensitivity were tested in vitro. Finally, paired pre-chemotherapy and post-chemotherapy omental HGSC specimens from patients were analyzed for neutrophil infiltration and NET formation.
resultsIn HGSC datasets, post-chemotherapy tumors exhibited increased IL1β expression with myeloid cells identified as the primary source. In chemoresistant murine models, chemotherapy increased neutrophils and NETs in omentum tumors in wild-type mice. These increases were abrogated in IL1β-deficient mice, which showed a shift toward an effector-like CD8
conclusionsWe demonstrate that chemotherapy-induced IL1β-dependent neutrophil accumulation drives chemoresistance in HGSC. This study provides experimental evidence that chemotherapy-induced inflammation contributes to chemoresistance and highlights the potential of targeting this pathway to overcome chemoresistance in HGSC.
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