INHBA(+) cancer-associated fibroblasts (CAFs) contribute to immunosuppression and tumor progression in ovarian cancer. This study identifies INHBA(+) CAFs as key players in promoting tumor growth and immunosuppression. In ovarian cancer mouse models, neutralizing Activin A reduced tumor progression and infiltration of pro-tumorigenic myofibroblasts and macrophages. INHBA(+) CAFs promote Treg differentiation through direct contact, which is mediated by SMAD2-dependent signaling that upregulates PD-L1. This study highlights the role of INHBA(+) CAFs in creating an immunosuppressive tumor microenvironment, suggesting that targeting these cells could be a potential therapeutic strategy for advanced ovarian cancers. The findings indicate that INHBA(+) CAFs are enriched in metastatic and recurrent ovarian cancers and are associated with poor patient survival. The study also shows that INHBA(+) CAFs are distinct from normal fibroblasts and are involved in the regulation of PD-L1, which is crucial for Treg differentiation and immunosuppression. The results suggest that targeting INHBA(+) CAFs could be a promising approach for improving immunotherapy outcomes in ovarian cancer.INHBA(+) cancer-associated fibroblasts (CAFs) contribute to immunosuppression and tumor progression in ovarian cancer. This study identifies INHBA(+) CAFs as key players in promoting tumor growth and immunosuppression. In ovarian cancer mouse models, neutralizing Activin A reduced tumor progression and infiltration of pro-tumorigenic myofibroblasts and macrophages. INHBA(+) CAFs promote Treg differentiation through direct contact, which is mediated by SMAD2-dependent signaling that upregulates PD-L1. This study highlights the role of INHBA(+) CAFs in creating an immunosuppressive tumor microenvironment, suggesting that targeting these cells could be a potential therapeutic strategy for advanced ovarian cancers. The findings indicate that INHBA(+) CAFs are enriched in metastatic and recurrent ovarian cancers and are associated with poor patient survival. The study also shows that INHBA(+) CAFs are distinct from normal fibroblasts and are involved in the regulation of PD-L1, which is crucial for Treg differentiation and immunosuppression. The results suggest that targeting INHBA(+) CAFs could be a promising approach for improving immunotherapy outcomes in ovarian cancer.