Changes in MAVS expression and T-cell infiltration in the tumor microenvironment following platinum-based chemotherapy in high-grade serous ovarian carcinoma

Background: High-grade serous ovarian carcinoma (HGSC) exhibits low sensitivity to immune checkpoint inhibitors (ICIs), partly due to limited tumor-infiltrating T cells. Type-I interferons (IFNs) from tumor cells may enhance T-cell infiltration. We investigated MAVS (mitochondrial antiviral-signaling protein) as an inducer of Type-I IFN signaling in HGSC and analyzed its association with immune-cell infiltration in relation to paclitaxel/carboplatin (TC) therapy and prognosis. Methods: We first included advanced HGSC cases at our institution that underwent interval debulking surgery (IDS) following neoadjuvant TC therapy. Paired pre-treatment biopsies and IDS specimens were collected for immunohistochemistry to evaluate MAVS expression in cancer cells and CD8⁺/CD4⁺ T-cell infiltration. Changes in MAVS expression and T-cell infiltration before and after TC therapy were analyzed, along with their correlation with sensitivity to TC. Next, using human HGSC cell lines, we assessed changes in MAVS expression and T-cell infiltration following platinum administration. Finally, we established an ID8 mouse model and divided mise into a cisplatin-treated group and a control group to compare the rate of ascites production and changes in body weight. We also compared immune-cell profiles in ascites (e.g., CD4⁺ and CD8⁺ T cells) and MAVS expression in tumor cells between each groups. Results: We analyzed 45 cases treated from December 1, 2019 to August 31, 2025. MAVS expression increased after TC therapy in most cases, and this increase correlated with enhanced CD8⁺ T-cell infiltration. In prognostic analyses, decreased MAVS expression after TC therapy was associated with poor prognostic features. In cell line experiments, MAVS expression was enhanced in platinum-treated cell lines, as demonstrated by Western blotting. In the ID8 mouse model, the rate of ascites production was faster in the cisplatin-treated group. We also visualized the proportions of immune cells within ascites in this group. Tumor cells derived from this model likewise exhibited increased MAVS expression in the cisplatin-treated group, as demonstrated by Western blotting. Conclusions: In HGSC, TC therapy-induced changes in MAVS expression may contribute to the induction of CD8⁺ T-cell infiltration. In vivo, platinum administration similarly suggested potential alterations in MAVS expression and immune-cell infiltration. MAVS may serve as a biomarker for patient selection in ICI therapy for HGSC.