捕食-被捕食者理论通常用于描述肿瘤在受到适应性免疫系统选择性压力的情况下的生长。这些相互作用由肿瘤免疫肽组与T细胞受体（TCR）库介导（肿瘤向身体"展示"的内容和身体"观察"癌细胞的能力）。肿瘤免疫肽组包括可以在肿瘤生成和治疗过程中获得和失去的新抗原。免疫肽组的异质性可预测某些肿瘤类型对免疫治疗反应不佳，表明TCR库无法支持对每个新抗原进行完全多克隆反应。重要的是，尽管已知肿瘤和T细胞群体之间相互竞争以获取肿瘤内资源，但外周T细胞之间的跨系竞争是否影响TCR库仍是未知的，也很难通过实验进行探究。计算模型可能提供一种研究这些现象并加深我们对肿瘤-免疫轴的理解的方式。在这里，我们构建了一个类似捕食-被捕食者的模型，并将其校准到临床前和临床数据中，以描述肿瘤的生长和免疫肽组的多样化。同时，我们模拟了抗原特异性T细胞谱系的扩展以及它们消耗谱系特异性抗原资源和谱系无关共享资源的情况。这个类似捕食-被捕食者的框架准确描述了临床观察到的免疫肽组，复制了与免疫治疗相关的效果，包括免疫编辑，并允许探索治疗生长和突变速率不同的肿瘤。版权：© 2023 Qi等。这是一篇开放获取文章，依据创作共用许可协议分发，只要原作者和出处被妥善标示，任何媒介都可以自由使用、分发和复制。

Predator-prey theory is commonly used to describe tumor growth in the presence of selective pressure from the adaptive immune system. These interactions are mediated by the tumor immunopeptidome (what the tumor "shows" the body) and the T-cell receptor (TCR) repertoire (how well the body "sees" cancer cells). The tumor immunopeptidome comprises neoantigens which can be gained and lost throughout tumorigenesis and treatment. Heterogeneity in the immunopeptidome is predictive of poor response to immunotherapy in some tumor types, suggesting that the TCR repertoire is unable to support a fully polyclonal response against every neoantigen. Importantly, while tumor and T-cell populations are known to compete with each other for intratumoral resources, whether between-lineage competition among peripheral T cells influences the TCR repertoire is unknown and difficult to interrogate experimentally. Computational models may offer a way to investigate these phenomena and deepen our understanding of the tumor-immune axis. Here, we construct a predator-prey-like model and calibrate it to preclinical and clinical data to describe tumor growth and immunopeptidome diversification. Simultaneously, we model the expansion of antigen-specific T-cell lineages and their consumption of both lineage-specific antigenic resources and lineage-agnostic, shared resources. This predator-prey-like framework accurately described clinically observed immunopeptidomes; recapitulated response-associated effects of immunotherapy, including immunoediting; and allowed exploration of treatment of tumors with varying growth and mutation rates.Copyright: © 2023 Qi et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.