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麻疹病毒向T细胞的高效MHC II类限制性呈递依赖于其靶向细胞受体人类CD46,并涉及内体途径。

Efficient MHC class II-restricted presentation of measles virus to T cells relies on its targeting to its cellular receptor human CD46 and involves an endosomal pathway.

作者信息

Gerlier D, Trescol-Biémont M C, Varior-Krishnan G, Naniche D, Fugier-Vivier I, Rabourdin-Combe C

机构信息

I.V.M.C., CNRS-UCBL UMR 30, Faculté Alexis Carrel, France.

出版信息

Cell Biol Int. 1994 May;18(5):315-20. doi: 10.1006/cbir.1994.1080.

Abstract

The role of the measles virus (MV) receptor, human CD46, in the uptake of MV and antigen presentation by Major Histocompatibility Complex (MHC) class II molecules was investigated. Expression of CD46 in murine B cells resulted in cells highly efficient in capturing UV-inactivated MV particles and presenting both envelope hemagglutinin H and nucleoprotein N to specific T cell hybridomas. Although MV fuse with the plasma membrane of its target cells, presentation of both MV-H and -N was sensitive to inhibition by chloroquine but was not affected by a tripeptide which prevents virus-cell fusion. Whereas 50 microM of chloroquine was required to inhibit presentation of MV-H, purified H or soluble N, only a two-fold lower concentration was required to inhibit that of MV-N. This shows that some CD46-mediated captured MV particles are endocytosed, then disrupted and processed in an endosome/lysosome compartment.

摘要

研究了麻疹病毒(MV)受体人类CD46在MV摄取以及主要组织相容性复合体(MHC)II类分子的抗原呈递中的作用。CD46在鼠B细胞中的表达导致细胞能够高效捕获紫外线灭活的MV颗粒,并将包膜血凝素H和核蛋白N呈递给特异性T细胞杂交瘤。尽管MV与靶细胞的质膜融合,但MV-H和-N的呈递对氯喹抑制敏感,而不受阻止病毒-细胞融合的三肽影响。抑制MV-H呈递需要50微摩尔氯喹,而抑制纯化的H或可溶性N的呈递也需要相同浓度的氯喹,但抑制MV-N的呈递所需浓度仅低两倍。这表明一些由CD46介导捕获的MV颗粒被内吞,然后在内体/溶酶体区室中被破坏和加工。

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