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MHC I类限制性抗原的体内交叉呈递需要TAP转运体。

In vivo cross-priming of MHC class I-restricted antigens requires the TAP transporter.

作者信息

Huang A Y, Bruce A T, Pardoll D M, Levitsky H I

机构信息

Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.

出版信息

Immunity. 1996 Apr;4(4):349-55. doi: 10.1016/s1074-7613(00)80248-4.

DOI:10.1016/s1074-7613(00)80248-4
PMID:8612129
Abstract

Recent in vitro evidence suggests two alternative mechanisms by which bone marrow-derived APCs may process exogenous antigens for presentation to CTL in vivo, a phenomenon termed cross-priming. Although in vitro studies have suggested that both TAP-dependent and TAP-independent pathways exist, we have now demonstrated an absolute requirement for a functional TAP for cross-priming to occur in vivo. Bone marrow chimeras reconstituted with marrow from TAP-defective donors develop functional CD8+ CTL, but have APCs with disrupted TAP function. In such chimeras, in vivo priming of naive CTL was observed when antigen was targeted to the ER in a TAP-independent fashion, but cross-priming could not be demonstrated. These results support the TAP-dependent mechanism of cross-priming.

摘要

最近的体外证据表明,骨髓来源的抗原呈递细胞(APC)可能通过两种替代机制在体内处理外源性抗原以呈递给细胞毒性T淋巴细胞(CTL),这一现象被称为交叉呈递。尽管体外研究表明存在TAP依赖性和TAP非依赖性途径,但我们现在已经证明,体内发生交叉呈递绝对需要功能性TAP。用来自TAP缺陷供体的骨髓重建的骨髓嵌合体可产生功能性CD8 + CTL,但APC的TAP功能被破坏。在这种嵌合体中,当抗原以TAP非依赖性方式靶向内质网时,可观察到幼稚CTL的体内致敏,但无法证明交叉呈递。这些结果支持交叉呈递的TAP依赖性机制。

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