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缺乏蛋白酶体亚基LMP-7的小鼠中MHC I类分子的表达

MHC class I expression in mice lacking the proteasome subunit LMP-7.

作者信息

Fehling H J, Swat W, Laplace C, Kühn R, Rajewsky K, Müller U, von Boehmer H

机构信息

Basel Institute for Immunology, Switzerland.

出版信息

Science. 1994 Aug 26;265(5176):1234-7. doi: 10.1126/science.8066463.

DOI:10.1126/science.8066463
PMID:8066463
Abstract

Proteasomes degrade endogenous proteins. Two subunits, LMP-2 and LMP-7, are encoded in a region of the major histocompatibility complex (MHC) that is critical for class I-restricted antigen presentation. Mice with a targeted deletion of the gene encoding LMP-7 have reduced levels of MHC class I cell-surface expression and present the endogenous antigen HY inefficiently; addition of peptides to splenocytes deficient in LMP-7 restores wild-type class I expression levels. This demonstrates the involvement of LMP-7 in the MHC class I presentation pathway and suggests that LMP-7 functions as an integral part of the peptide supply machinery.

摘要

蛋白酶体可降解内源性蛋白质。其中两个亚基,即LMP - 2和LMP - 7,由主要组织相容性复合体(MHC)的一个区域编码,该区域对于I类限制性抗原呈递至关重要。靶向缺失编码LMP - 7基因的小鼠,其MHC I类细胞表面表达水平降低,且内源性抗原HY呈递效率低下;向缺乏LMP - 7的脾细胞中添加肽可恢复野生型I类表达水平。这证明了LMP - 7参与MHC I类呈递途径,并表明LMP - 7作为肽供应机制的一个组成部分发挥作用。

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