LAUSR

Highlights • Systemic knockdown of the long form prolactin receptor in vivo increases survival in an aggressive, immunocompetent model of stage IV, triple negative breast cancer.• Knockdown of the long form prolactin receptor reduces Treg recruitment to tumors by reducing tumor parenchymal production of CCL-17.• Those Tregs still recruited to primary tumors have a substantial reduction in their ability to promote epithelial to mesenchymal transition of tumor parenchyma.• For the Tregs in the primary tumor, there is transcript downregulation of components of the T cell receptor complex and CTLA-4.• Tregs outside of the tumor have normal ability to suppress T effector cell proliferation after 1–5 months of treatment.• Knockdown of the long form of the prolactin receptor therefore seems to have an intra-tumor immunotherapeutic effect without effect on peripheral Treg function.