| pubmed-article:10839811 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10839811 | lifeskim:mentions | umls-concept:C0567416 | lld:lifeskim |
| pubmed-article:10839811 | lifeskim:mentions | umls-concept:C0003320 | lld:lifeskim |
| pubmed-article:10839811 | lifeskim:mentions | umls-concept:C0017968 | lld:lifeskim |
| pubmed-article:10839811 | lifeskim:mentions | umls-concept:C0597361 | lld:lifeskim |
| pubmed-article:10839811 | lifeskim:mentions | umls-concept:C0024518 | lld:lifeskim |
| pubmed-article:10839811 | lifeskim:mentions | umls-concept:C1257986 | lld:lifeskim |
| pubmed-article:10839811 | lifeskim:mentions | umls-concept:C0456387 | lld:lifeskim |
| pubmed-article:10839811 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:10839811 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:10839811 | pubmed:dateCreated | 2000-8-3 | lld:pubmed |
| pubmed-article:10839811 | pubmed:abstractText | Heat shock proteins (HSPs) like glycoprotein (gp)96 (glucose-regulated protein 94 [grp94]) are able to induce specific cytotoxic T lymphocyte (CTL) responses against cells from which they originate. Here, we demonstrate that for CTL activation by gp96-chaperoned peptides, specific receptor-mediated uptake of gp96 by antigen-presenting cells (APCs) is required. Moreover, we show that in both humans and mice, only professional APCs like dendritic cells (DCs), macrophages, and B cells, but not T cells, are able to bind gp96. The binding is saturable and can be inhibited using unlabeled gp96 molecules. Receptor binding by APCs leads to a rapid internalization of gp96, which colocalizes with endocytosed major histocompatibility complex (MHC) class I and class II molecules in endosomal compartments. Incubation of gp96 molecules isolated from cells expressing an adenovirus type 5 E1B epitope with the DC line D1 results in the activation of E1B-specific CTLs. This CTL activation can be specifically inhibited by the addition of irrelevant gp96 molecules not associated with E1B peptides. Our results demonstrate that only receptor-mediated endocytosis of gp96 molecules leads to MHC class I-restricted re-presentation of gp96-associated peptides and CTL activation; non-receptor-mediated, nonspecific endocytosis is not able to do so. Thus, we provide evidence on the mechanisms by which gp96 is participating in the cross-presentation of antigens from cellular origin. | lld:pubmed |
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| pubmed-article:10839811 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10839811 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10839811 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10839811 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10839811 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:10839811 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:10839811 | pubmed:author | pubmed-author:Ricciardi-Cas... | lld:pubmed |
| pubmed-article:10839811 | pubmed:author | pubmed-author:SchildHH | lld:pubmed |
| pubmed-article:10839811 | pubmed:author | pubmed-author:RaniRR | lld:pubmed |
| pubmed-article:10839811 | pubmed:author | pubmed-author:RammenseeH... | lld:pubmed |
| pubmed-article:10839811 | pubmed:author | pubmed-author:NeefjesJJ | lld:pubmed |
| pubmed-article:10839811 | pubmed:author | pubmed-author:ToesR ERE | lld:pubmed |
| pubmed-article:10839811 | pubmed:author | pubmed-author:HiklWW | lld:pubmed |
| pubmed-article:10839811 | pubmed:author | pubmed-author:SchoenbergerS... | lld:pubmed |
| pubmed-article:10839811 | pubmed:author | pubmed-author:SpeePP | lld:pubmed |
| pubmed-article:10839811 | pubmed:author | pubmed-author:Arnold-Schild... | lld:pubmed |
| pubmed-article:10839811 | pubmed:author | pubmed-author:Singh-JasujaH... | lld:pubmed |
| pubmed-article:10839811 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10839811 | pubmed:day | 5 | lld:pubmed |
| pubmed-article:10839811 | pubmed:volume | 191 | lld:pubmed |
