Abstract Cancer recurrence presents a huge challenge in cancer patient management. Immune escape is a key mechanism of cancer progression and metastatic dissemination. CD25 is expressed in regulatory T (Treg) cells including tumor-infiltrating Treg cells (TI-Tregs). These cells specially activate and reinforce immune escape mechanism of cancers. The suppression of CD25/IL-2 interaction would be useful against Treg cells activation and ultimately immune escape of cancer. Here, software, web servers and databases were used, at which in silico designed small interfering RNAs (siRNAs), de novo designed peptides and virtual screened small molecules against CD25 were introduced for the prospect of eliminating cancer immune escape and obtaining successful treatment. We obtained siRNAs with low off-target effects. Further, small molecules based on the binding homology search in ligand and receptor similarity were introduced. Finally, the critical amino acids on CD25 were targeted by a de novo designed peptide with disulfide bond. Hence we introduced computational-based antagonists to lay a foundation for further in vitro and in vivo studies.

中文翻译：

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抑制 CD25/IL-2 相互作用的计算研究

摘要 癌症复发对癌症患者的管理提出了巨大的挑战。免疫逃逸是癌症进展和转移传播的关键机制。CD25 在调节性 T (Treg) 细胞中表达，包括肿瘤浸润性 Treg 细胞 (TI-Treg)。这些细胞专门激活和加强癌症的免疫逃逸机制。CD25/IL-2 相互作用的抑制将有助于对抗 Treg 细胞活化和最终的癌症免疫逃逸。在这里，使用软件、网络服务器和数据库，在其中计算机设计了小干扰 RNA (siRNAs)，从头设计肽和针对 CD25 的虚拟筛选小分子被引入，以期消除癌症免疫逃逸并获得成功治疗。我们获得了低脱靶效应的siRNA。更多，引入了基于配体和受体相似性中结合同源性搜索的小分子。最后，CD25 上的关键氨基酸被从头设计的具有二硫键的肽靶向。因此，我们引入了基于计算的拮抗剂，为进一步的体外和体内研究奠定了基础。