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本文引用的文献

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Broad cross-reactive TCR repertoires recognizing dissimilar Epstein-Barr and influenza A virus epitopes.广泛交叉反应的 TCR 库识别不同的 Epstein-Barr 和流感 A 病毒表位。
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IFN-induced attrition of CD8 T cells in the presence or absence of cognate antigen during the early stages of viral infections.在病毒感染早期阶段,无论有无同源抗原存在时,干扰素诱导的CD8 T细胞损耗。
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Cross-reactive influenza virus-specific CD8+ T cells contribute to lymphoproliferation in Epstein-Barr virus-associated infectious mononucleosis.交叉反应性流感病毒特异性CD8 + T细胞促成了爱泼斯坦-巴尔病毒相关传染性单核细胞增多症中的淋巴细胞增殖。
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Turnover rates of B cells, T cells, and NK cells in simian immunodeficiency virus-infected and uninfected rhesus macaques.感染和未感染猿猴免疫缺陷病毒的恒河猴中B细胞、T细胞和NK细胞的周转率
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A systematic approach to vaccine complexity using an automaton model of the cellular and humoral immune system. I. Viral characteristics and polarized responses.一种使用细胞和体液免疫系统自动机模型研究疫苗复杂性的系统方法。I. 病毒特征与极化反应。
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一种免疫系统的离散计算机模型揭示了体液免疫分支与细胞免疫分支之间以及交叉反应记忆和初始反应之间的竞争性相互作用。

A discrete computer model of the immune system reveals competitive interactions between the humoral and cellular branch and between cross-reacting memory and naïve responses.

作者信息

Cheng Yiming, Ghersi Dario, Calcagno Claudia, Selin Liisa K, Puzone Roberto, Celada Franco

机构信息

Department of Medicine, New York University School of Medicine, New York, NY, USA.

出版信息

Vaccine. 2009 Feb 5;27(6):833-45. doi: 10.1016/j.vaccine.2008.11.109. Epub 2008 Dec 25.

DOI:10.1016/j.vaccine.2008.11.109
PMID:19101600
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3905836/
Abstract

In an agent-based computer model, we simulate the formation and recall of anti-virus immunological memory. Specifically we try to predict what will happen, both to the response and to memory, when the second infecting virus is partly different from the first one, and when the cross-reactivity of the two branches of the immune system (IS), humoral and cellular, is asymmetrical, or "split". The simulations explore systematically epitope distances, and measure all changes in affinity, cellularity and efficiency in clearing the infection. Besides obvious cooperation, they reveal powerful competitions between the branches, and more intriguing, between cross-reacting and new responses when the latter suffer the competition by preformed cell-rich but inefficient clones, as memory, usually an asset, becomes a liability.

摘要

在一个基于主体的计算机模型中,我们模拟了抗病毒免疫记忆的形成与回忆。具体而言,我们试图预测当第二次感染的病毒与第一次部分不同时,以及当免疫系统(IS)的两个分支,即体液免疫和细胞免疫的交叉反应不对称或“分裂”时,反应和记忆会发生什么情况。模拟系统地探索了表位距离,并测量了清除感染过程中亲和力、细胞数量和效率的所有变化。除了明显的协同作用外,它们还揭示了两个分支之间强大的竞争,更有趣的是,当新的反应受到预先形成的、细胞丰富但效率低下的克隆(作为记忆,通常是一种资产)的竞争时,交叉反应和新反应之间的竞争,此时记忆变成了一种负担。

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