报告题目：Original Antigenic Sin in CD4+ T Cells

报告人：马君岭教授(加拿大维多利亚大学)

报告时间：2025年5月29日(10:00-11:00)

报告地点：复杂系统研究所四层(409)

报告人简介：马君岭，1997年获西安交通大学应用数学硕士学位，2003年获普林斯顿大学(Princeton University)应用数学博士学位，师从美国科学院院士Simon Levin教授，现任加拿大维多利亚大学(University of Victoria)数学与统计系教授，主持多项加拿大理事会或基金会项目，其研究内容主要包括社交网络上传染病传播的建模和最优控制策略、对随机网络上扩散过程的建模研究以及对流感、艾滋病毒、埃博拉和霍乱等具体传染病的建模和研究，已经在Nature Communications、Bulletin of Mathematical Biology、 Journal of Mathematical Biology等国际著名期刊上发表高水平论文30余篇。

报告人摘要：Original antigenic sin (OAS) is the phenomenon where prior exposure to an antigen results in a decreased adaptive antibody response to a heterologous infection. This phenomenon may negatively impact the effectiveness of immunity acquired from vaccination or previous infections. We demonstrate that this phenomenon arises because the proliferation and regulation signals of CD4+ T cells are antigen-nonspecific. Fast-responding memory CD4+ T cells trigger a regulatory T cell (Treg) response, which prematurely suppresses the naive CD4+ T cell response, leading to a similar OAS effect in CD4+ T cells. We illustrate this mechanism using a mathematical model that incorporates the proliferation of naive and memory CD4+ T cells, interleukin-2 (lL-2), and Tregs. Our model is calibrated with experimental data and uses numerical simulations to study how the CD4+ T cell response varies with the level of cross-reactivity between memory CD4+ T cells and the antigen causing the secondary infection. Our results indicate that the immune response is weakest at an intermediate level of cross-reactivity, a key feature of OAS. This mechanism can also explain OAS in antibody responses.

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