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T细胞交叉呈递中的抗原偏向性。

Antigen bias in T cell cross-priming.

作者信息

Wolkers Monika C, Brouwenstijn Nathalie, Bakker Arnold H, Toebes Mireille, Schumacher Ton N M

机构信息

Division of Immunology, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, Netherlands.

出版信息

Science. 2004 May 28;304(5675):1314-7. doi: 10.1126/science.1096268.

DOI:10.1126/science.1096268
PMID:15166378
Abstract

Activated CD8+ T cells detect virally infected cells and tumor cells by recognition of major histocompatibility complex class I-bound peptides derived from degraded, endogenously produced proteins. In contrast, CD8+ T cell activation often occurs through interaction with specialized antigen-presenting cells displaying peptides acquired from an exogenous cellular source, a process termed cross-priming. Here, we observed a marked inefficiency in exogenous presentation of epitopes derived from signal sequences in mouse models. These data indicate that certain virus- and tumor-associated antigens may not be detected by CD8+ T cells because of impaired cross-priming. Such differences in the ability to cross-present antigens should form important considerations in vaccine design.

摘要

活化的CD8 + T细胞通过识别源自降解的内源性产生的蛋白质的主要组织相容性复合体I类结合肽来检测病毒感染细胞和肿瘤细胞。相比之下,CD8 + T细胞活化通常通过与展示从外源细胞来源获得的肽的特化抗原呈递细胞相互作用而发生,这一过程称为交叉呈递。在这里,我们在小鼠模型中观察到源自信号序列的表位的外源呈递存在明显的低效率。这些数据表明,由于交叉呈递受损,某些病毒和肿瘤相关抗原可能无法被CD8 + T细胞检测到。抗原交叉呈递能力的这种差异应成为疫苗设计中的重要考虑因素。

相似文献

1
Antigen bias in T cell cross-priming.T细胞交叉呈递中的抗原偏向性。
Science. 2004 May 28;304(5675):1314-7. doi: 10.1126/science.1096268.
2
CD8+ T cell cross-priming via transfer of proteasome substrates.通过蛋白酶体底物转移实现的CD8 + T细胞交叉启动
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Immunology. Nothing 'gainst time's scythe can make defense..免疫学。没有什么能抵御时间的镰刀。
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CTL induction by cross-priming is restricted to immunodominant epitopes.通过交叉呈递诱导的细胞毒性T淋巴细胞(CTL)仅限于免疫显性表位。
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Cross-priming of CD8+ T cells by viral and tumor antigens is a robust phenomenon.病毒和肿瘤抗原对CD8 + T细胞的交叉呈递是一种显著现象。
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Increased antigen cross-presentation but impaired cross-priming after activation of peroxisome proliferator-activated receptor gamma is mediated by up-regulation of B7H1.过氧化物酶体增殖物激活受体γ激活后,抗原交叉呈递增加但交叉启动受损,这是由B7H1上调介导的。
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Toll-like receptor 3 promotes cross-priming to virus-infected cells.Toll样受体3促进对病毒感染细胞的交叉启动。
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