| pubmed-article:9432982 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9432982 | lifeskim:mentions | umls-concept:C0024518 | lld:lifeskim |
| pubmed-article:9432982 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
| pubmed-article:9432982 | lifeskim:mentions | umls-concept:C1704241 | lld:lifeskim |
| pubmed-article:9432982 | lifeskim:mentions | umls-concept:C0456387 | lld:lifeskim |
| pubmed-article:9432982 | lifeskim:mentions | umls-concept:C1522492 | lld:lifeskim |
| pubmed-article:9432982 | lifeskim:mentions | umls-concept:C0205227 | lld:lifeskim |
| pubmed-article:9432982 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
| pubmed-article:9432982 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:9432982 | pubmed:dateCreated | 1998-2-3 | lld:pubmed |
| pubmed-article:9432982 | pubmed:abstractText | Efficient loading of major histocompatibility complex class II molecules with peptides requires the invariant chain (Ii) and the class II-like molecule H-2M. Recent in vitro biochemical studies suggest that H2-M may function as a chaperone to rescue empty class II dimers. To test this hypothesis in vivo, we generated mice lacking both Ii and H-2M (Ii-/-M-/-). Antigen presenting cells (APCs) from Ii-/-M-/- mice, as compared with APCs from Ii-/- mice, exhibit a significant reduction in their ability to present self-peptides to a panel of class II I-Ab-restricted T cells. As a consequence of this defect in the loading of self peptides, CD4(+) thymocyte development is profoundly impaired in Ii-/-M-/- mice, resulting in a peripheral CD4(+) T cell population with low levels of T cell receptor expression. These findings are consistent with the idea that H-2M functions as a chaperone in the peptide loading of class II molecules in vivo. | lld:pubmed |
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| pubmed-article:9432982 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:9432982 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9432982 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9432982 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:9432982 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:9432982 | pubmed:author | pubmed-author:EastmanSS | lld:pubmed |
| pubmed-article:9432982 | pubmed:author | pubmed-author:RudenskyA YAY | lld:pubmed |
| pubmed-article:9432982 | pubmed:author | pubmed-author:GrubinC ECE | lld:pubmed |
| pubmed-article:9432982 | pubmed:author | pubmed-author:Van KaerLL | lld:pubmed |
| pubmed-article:9432982 | pubmed:author | pubmed-author:KovatsSS | lld:pubmed |
| pubmed-article:9432982 | pubmed:author | pubmed-author:deRoosPP | lld:pubmed |
| pubmed-article:9432982 | pubmed:author | pubmed-author:DongreAA | lld:pubmed |
| pubmed-article:9432982 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9432982 | pubmed:day | 19 | lld:pubmed |
| pubmed-article:9432982 | pubmed:volume | 187 | lld:pubmed |
| pubmed-article:9432982 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9432982 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9432982 | pubmed:pagination | 245-51 | lld:pubmed |
| pubmed-article:9432982 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:9432982 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9432982 | pubmed:articleTitle | Invariant chain-independent function of H-2M in the formation of endogenous peptide-major histocompatibility complex class II complexes in vivo. | lld:pubmed |
| pubmed-article:9432982 | pubmed:affiliation | Department of Immunology, University of Washington School of Medicine, Seattle 98195, USA. | lld:pubmed |
| pubmed-article:9432982 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9432982 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:9432982 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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