Galassi Claudia, Petroni Giulia, Knott Simon R V, Galluzzi Lorenzo
Department of Pharmacology, Weill Cornell Medical College, New York, NY, USA.
Department of Experimental and Clinical Medicine, University of Florence, Florence, Italy.
Oncoimmunology. 2025 Dec;14(1):2520269. doi: 10.1080/2162402X.2025.2520269. Epub 2025 Jul 15.
CDK4/6 inhibitors are central to the clinical management of HRHER2 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.
细胞周期蛋白依赖性激酶4/6（CDK4/6）抑制剂是激素受体阳性（HR）/人表皮生长因子受体2阴性（HER2）乳腺癌临床管理的核心。我们最近证明，在CDK4/6抑制后，通过CCL2依赖性机制募集到肿瘤微环境中的分泌白细胞介素17（IL17）的免疫抑制性γδT细胞可使肿瘤相关巨噬细胞重新极化，使其朝向与治疗耐药相关的CX3CR1表型。
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