Breast cancer (BC) is widely recognized as a prevalent contributor to cancer mortality and ranks as the second most prevalent form of cancer among women across the globe. Hence, the development of innovative therapeutic strategies is imperative to effectively manage BC. The B- and T-lymphocyte attenuator (BTLA)–Herpesvirus entry mediator (HVEM) complex has garnered significant scientific interest as a crucial regulator in various immune contexts. The interaction between BTLA–HVEM ligand on the surface of T cells results in reduced cellular activation, cytokine synthesis, and proliferation. The BTLA–HVEM complex has been investigated in various cancers, yet its specific mechanisms in BC remain indeterminate. In this study, we aim to examine the function of BTLA–HVEM and provide a comprehensive overview of the existing evidence in relation to BC. The obstruction or augmentation of these pathways may potentially enhance the efficacy of BC treatment.

乳腺癌 (BC) 被广泛认为是癌症死亡率的一个常见原因，并且是全球女性中第二常见的癌症。因此，开发创新的治疗策略对于有效管理 BC 势在必行。 B 淋巴细胞和 T 淋巴细胞衰减因子 (BTLA)-疱疹病毒进入介质 (HVEM) 复合物作为各种免疫环境中的关键调节因子，引起了重大科学兴趣。 T 细胞表面的 BTLA-HVEM 配体之间的相互作用导致细胞活化、细胞因子合成和增殖减少。 BTLA-HVEM 复合物已在多种癌症中进行了研究，但其在 BC 中的具体机制仍不确定。在本研究中，我们旨在检查 BTLA-HVEM 的功能，并全面概述与 BC 相关的现有证据。这些途径的阻塞或增强可能会增强 BC 治疗的功效。