Objective：This study aimed to investigate the lipid metabolism characteristics，particularly lipid uptake and accumulation of regulatory CD4 + T cells（Treg）in the ovarian cancer microenvironment，and its potential impact on the expression of programmed cell death protein 1（PD - 1）and lymphocyte associated protein 4（CTLA - 4）. Methods：The lipophilic fluorescent dye BODIPYTM 493/503 and the fluorescent fatty acid probe BODIPY™ 500/510 C1 C12 were used to detect intracellular lipid content and lipid uptake capacity，respectively，in human CD4 + Tregs isolated from ovarian cancer tissues or co -cultured with supernatants from various ovarian cancer cell lines（ES -2，SKOV3，CAOV3）. Lipid metabolism was modulated using the fatty acid oxidation inhibitor Etomoxir，the fatty acid synthesis inhibitor C75，and the fatty acid uptake inhibitor sulfo-N-succinimidyl oleate（SSO）. Lipid content and the expression of immunosuppressive molecules PD - 1 and CTLA - 4 were analyzed by flow cytometry. Results：CD4 + Treg infiltrating ovarian cancer tissues exhibited significantly higher lipid content and lipid uptake capacity compared to conventional CD4+ T cells（P ＜ 0.01）. Among the ovarian cancer tumor supernatant tested in vitro，CAOV3-derived supernatant most significantly enhanced intracellular lipid content and uptake capacity in CD4 + Treg relative to basal medium（P ＜ 0.05）. Furthermore，CAOV3-conditioned medium upregulated PD - 1 and CTLA -4 expression in CD4 + Treg（P ＜ 0.05）. This was accompanied by a concentration - dependent increase in both lipid accumulation and fluorescent fatty acid analog uptake（P ＜ 0.05）. Notably，the fatty acid uptake inhibitor SSO effectively reversed the CAOV3 supernatant-induced lipid accumulation（P ＜ 0.05）in CD4+ Treg and the elevated expression of PD-1 and CTLA - 4（all P ＜ 0.05），whereas the oxidation inhibitor Etomoxir and the synthesis inhibitor C75 had no significant effect. Conclusion：The ovarian cancer microenvironment promotes lipid uptake in CD4 + Tregs，leading to intracellular lipid droplet accumulation，which in turn enhances their immunosuppressive function，as evidenced by upregulated PD-1 and CTLA-4 expression. Targeting the fatty acid uptake pathway may represent a potential strategy to reverse Treg - mediated immunosuppression in ovarian cancer.