Dendritic Cell Activation Prevents MHC Class II Ubiquitination and Promotes MHC Class II Survival Regardless of the Activation Stimulus

被引：42

作者：

Walseng, Even ^{[1
]}

Furuta, Kazuyuki ^{[1
]}

Goldszmid, Romina S. ^{[2
,3
]}

Weih, Karis A. ^{[1
]}

Sher, Alan ^{[2
]}

Roche, Paul A. ^{[1
]}

机构：

[1] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA

[2] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA

[3] NCI, Expt Immunol Lab, Canc & Inflammat Program, Ctr Canc Res,NIH, Frederick, MD 21702 USA

来源：

JOURNAL OF BIOLOGICAL CHEMISTRY | 2010年 / 285卷 / 53期

基金：

美国国家卫生研究院;

关键词：

TOXOPLASMA-GONDII; PLASMA-MEMBRANE; COMPLEXES; SURFACE; EXPRESSION; MATURATION; INFECTION; TRANSPORT; PARASITES; FUSION;

D O I：

10.1074/jbc.M110.157586

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The expression of MHC class II (MHC-II) on the surface of antigen-presenting cells, such as dendritic cells (DCs), is tightly regulated during cellular activation. Many cells, including DCs, are activated following stimulation of innate Toll-like receptors (TLRs) by products of microorganisms. In the resting (immature) state, MHC-II is ubiquitinated in immature DCs and is rapidly degraded; however, after activation of these cells with MyD88-dependent TLR ligands, MHC-II ubiquitination is blocked, and MHC-II survival is prolonged. We now show that DC activation using MyD88-dependent TLR ligands, MyD88-independent TLR ligands, and even infection with the intracellular parasite Toxoplasma gondii leads to identical changes in MHC-II expression, ubiquitination, and surface stability, revealing a conserved role for enhanced MHC-II stability after DC activation by different stimuli.

引用

页码：41749 / 41754

页数：6

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