HR+乳腺癌对CDK4/6抑制剂耐药的免疫学机制

IF 6.5 2区医学 Q1 IMMUNOLOGY

Oncoimmunology Pub Date : 2025-12-01 Epub Date: 2025-07-15 DOI:10.1080/2162402X.2025.2520269

Claudia Galassi, Giulia Petroni, Simon R V Knott, Lorenzo Galluzzi

引用次数: 0

摘要

CDK4/6抑制剂是HR+HER2-乳腺癌临床治疗的核心。我们最近证明，免疫抑制，分泌il17的γδ T细胞通过CDK4/6抑制的ccl2依赖机制募集到肿瘤微环境中，可以将肿瘤相关巨噬细胞重新极化为与治疗耐药相关的CX3CR1+表型。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

An immunological mechanism of resistance to CDK4/6 inhibitors in HR<sup>+</sup> breast cancer.

查看原文本刊更多论文

An immunological mechanism of resistance to CDK4/6 inhibitors in HR⁺ breast cancer.

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.

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来源期刊

Oncoimmunology ONCOLOGYIMMUNOLOGY-IMMUNOLOGY

CiteScore

12.50

自引率

2.80%

发文量

276

审稿时长

24 weeks

期刊介绍： OncoImmunology is a dynamic, high-profile, open access journal that comprehensively covers tumor immunology and immunotherapy. As cancer immunotherapy advances, OncoImmunology is committed to publishing top-tier research encompassing all facets of basic and applied tumor immunology. The journal covers a wide range of topics, including: -Basic and translational studies in immunology of both solid and hematological malignancies -Inflammation, innate and acquired immune responses against cancer -Mechanisms of cancer immunoediting and immune evasion -Modern immunotherapies, including immunomodulators, immune checkpoint inhibitors, T-cell, NK-cell, and macrophage engagers, and CAR T cells -Immunological effects of conventional anticancer therapies.