A PHAGOSOME-TO-CYTOSOL PATHWAY FOR EXOGENOUS ANTIGENS PRESENTED ON MHC CLASS-I MOLECULES
A PHAGOSOME-TO-CYTOSOL PATHWAY FOR EXOGENOUS ANTIGENS PRESENTED ON MHC CLASS-I MOLECULES
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DOI：
10.1126/science.7809629
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发表时间：
1995-01-13
期刊：
影响因子：
56.9
通讯作者：
ROCK, KL
中科院分区：
文献类型：
--
作者：
KOVACSOVICSBANKOWSKI, M;ROCK, KL
来自内源性蛋白质的多肽是由主要的组织相容性复合体I类分子提呈的，而胞外液中的抗原通常不是。然而，病原体或颗粒抗原内化到巨噬细胞(MO)的吞噬小体中，刺激CD8T细胞。这些AGS的呈递对氯喹具有抵抗力，但可被蛋白酶体的抑制剂、TAP1-TAP2转运体的突变和布雷菲尔丁A阻断。此外，吞噬核糖体失活蛋白抑制MM蛋白的合成。这些结果表明，MOS将AGS从吞噬小体转移到胞浆中，内源和外源AGS使用最终的共同途径来呈现I类。
Peptides from endogenous proteins are presented by major histocompatibility complex class I molecules, but antigens (Ags) in the extracellular fluids are generally not. However, pathogens or particulate Ags that are internalized into phagosomes of macrophages (MOs) stimulate CD8 T cells. The presentation of these Ags is resistant to chloroquine but is blocked by inhibitors of the proteasome, a mutation in the TAP1-TAP2 transporter, and brefeldin A. Moreover, phagocytosis of a ribosomal-inactivating protein inhibited MM protein synthesis. These results demonstrate that MOs transfer Ags from phagosomes into the cytosol and that endogenous and exogenous Ags use a final common pathway for class I presentation.