上皮间充质转化（EMT）在胚胎发育、组织纤维化、修复和肿瘤侵袭中起着关键作用。新兴的研究强调了EMT与免疫检查点分子，尤其是程序性细胞死亡配体1（PDL1）之间的密切关联。PDL1通过双向调控对EMT产生影响。EMT相关因子，如YB1，通过直接结合其启动子来增强PDL1表达。相反，PDL1信号触发下游通路，如PI3K/AKT和MAPK，促进EMT并促进癌细胞迁移和侵袭。针对PDL1的治疗具有治疗EMT相关疾病，包括癌症和纤维化的潜力。事实上，PDL1抑制剂，如pembrolizumab和nivolumab，在各种癌症的临床试验中已显示出有希望的结果。最近的研究还表明，它们在纤维化治疗中减少成纤维细胞活化和细胞外基质沉积方面具有潜在的益处，从而解决纤维化问题。在本综述中，我们探讨了PDL1在免疫调节、生长和纤维化促进中的多方面作用。我们讨论了与PDL1相关的挑战、机制和临床观察，包括治疗中PD1/PDL1轴的局限性和PD1独立内在PDL1信号的限制。我们的研究强调了在不同肿瘤类型中EMT过程中PDL1表达的动态变化。通过PDL1与EMT之间的相互作用，我们揭示了共向性改变、调控途径和PDL1干预在肿瘤学中产生的各种不同变化。此外，我们的发现强调了PDL1在促进纤维化和调节免疫反应方面的双重作用，对治疗方法具有潜在的影响。我们特别研究了在II型EMT纤维化中靶向PDL1的治疗潜力：在纤维化调控和免疫反应调节之间取得平衡。这个分析提供了有关PDL1多方面功能的有价值见解，并有助于我们理解其复杂机制和治疗意义。版权所有©2023张、张、王、赵和何。

Epithelial-mesenchymal transformation (EMT) plays a pivotal role in embryonic development, tissue fibrosis, repair, and tumor invasiveness. Emerging studies have highlighted the close association between EMT and immune checkpoint molecules, particularly programmed cell death ligand 1 (PDL1). PDL1 exerts its influence on EMT through bidirectional regulation. EMT-associated factors, such as YB1, enhance PDL1 expression by directly binding to its promoter. Conversely, PDL1 signaling triggers downstream pathways like PI3K/AKT and MAPK, promoting EMT and facilitating cancer cell migration and invasion. Targeting PDL1 holds promise as a therapeutic strategy for EMT-related diseases, including cancer and fibrosis. Indeed, PDL1 inhibitors, such as pembrolizumab and nivolumab, have shown promising results in clinical trials for various cancers. Recent research has also indicated their potential benefit in fibrosis treatment in reducing fibroblast activation and extracellular matrix deposition, thereby addressing fibrosis. In this review, we examine the multifaceted role of PDL1 in immunomodulation, growth, and fibrosis promotion. We discuss the challenges, mechanisms, and clinical observations related to PDL1, including the limitations of the PD1/PDL1 axis in treatment and PD1-independent intrinsic PDL1 signaling. Our study highlights the dynamic changes in PDL1 expression during the EMT process across various tumor types. Through interplay between PDL1 and EMT, we uncover co-directional alterations, regulatory pathways, and diverse changes resulting from PDL1 intervention in oncology. Additionally, our findings emphasize the dual role of PDL1 in promoting fibrosis and modulating immune responses across multiple diseases, with potential implications for therapeutic approaches. We particularly investigate the therapeutic potential of targeting PDL1 in type II EMT fibrosis: strike balance between fibrosis modulation and immune response regulation. This analysis provides valuable insights into the multifaceted functions of PDL1 and contributes to our understanding of its complex mechanisms and therapeutic implications.Copyright © 2023 Zhang, Zhang, Wang, Zhao and He.