An immunological mechanism of resistance to CDK4/6 inhibitors in HR+ breast cancer.
Editorial Article
Overview
abstract
CDK4/6 inhibitors are central to the clinical management of HR+HER2- breast cancer. We have recently demonstrated that immunosuppressive, IL17-secreting γδ T cells recruited to the tumor microenvironment by a CCL2-dependent mechanism upon CDK4/6 inhibition can repolarize tumor-associated macrophages toward a CX3CR1+ phenotype associated with resistance to therapy.
