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- W4308381799 abstract "<h3>Background</h3> Initiation of an immune response requires activation of one or more naïve T cells. Each naïve T cell has a unique T cell receptor, and these cells traffic through the blood and lymphatic vasculatures, visiting each of the ~500 lymph nodes in search of matching antigen. If a match is made, then the naïve T cell activates and proliferates. This process is potentially rate-limiting, given the few naive T cells capable of recognizing tumor antigen and the random nature of their entry into each lymph node. We propose that stochastic nature of this process affects the probability of T cell activation and may contribute to the poor response to ICB therapy seen in most patients. <h3>Methods</h3> Here, we use multiscale computational modeling to identify potential reasons for clinical failure of immune checkpoint therapies and develop strategies for improving naïve T cell activation and tumor killing. The model provides a mechanistic framework for optimizing cancer immunotherapy and developing testable solutions to unleash anti-tumor immune responses for more patients with cancer. <h3>Results</h3> The results show that tumor antigen production rate is a critical parameter, and that patients with low tumor antigen production rate need additional treatment to enhance antigen level and improve immune checkpoint inhibition therapy. <h3>Conclusions</h3> The co-localization of antigen with appropriate naive T cells is a critical step in immune activation, and affects the anti-tumor response in the context of immune checkpoint therapy." @default.
- W4308381799 created "2022-11-11" @default.
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- W4308381799 date "2022-11-01" @default.
- W4308381799 modified "2023-10-14" @default.
- W4308381799 title "1295 Systems biology analysis of anti-tumor immunity" @default.
- W4308381799 doi "https://doi.org/10.1136/jitc-2022-sitc2022.1295" @default.
- W4308381799 hasPublicationYear "2022" @default.
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