| pubmed-article:9256471 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9256471 | lifeskim:mentions | umls-concept:C1512631 | lld:lifeskim |
| pubmed-article:9256471 | lifeskim:mentions | umls-concept:C1848980 | lld:lifeskim |
| pubmed-article:9256471 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:9256471 | lifeskim:mentions | umls-concept:C0868955 | lld:lifeskim |
| pubmed-article:9256471 | lifeskim:mentions | umls-concept:C1326202 | lld:lifeskim |
| pubmed-article:9256471 | lifeskim:mentions | umls-concept:C0686907 | lld:lifeskim |
| pubmed-article:9256471 | pubmed:issue | 17 | lld:pubmed |
| pubmed-article:9256471 | pubmed:dateCreated | 1997-9-17 | lld:pubmed |
| pubmed-article:9256471 | pubmed:abstractText | In pre-B lymphocytes, productive rearrangement of Ig light chain genes allows assembly of the B cell receptor (BCR), which selectively promotes further developmental maturation through poorly defined transmembrane signaling events. Using a novel in vitro system to study immune tolerance during development, we find that BCR reactivity to auto-antigen blocks this positive selection, preventing down-regulation of light chain gene recombination and promoting secondary light chain gene rearrangements that often alter BCR specificity, a process called receptor editing. Under these experimental conditions, self-antigen induces secondary light chain gene rearrangements in at least two-thirds of autoreactive immature B cells, but fails to accelerate cell death at this stage. These data suggest that in these cells the mechanism of immune tolerance is receptor selection rather than clonal selection. | lld:pubmed |
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| pubmed-article:9256471 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:9256471 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9256471 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9256471 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:9256471 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:9256471 | pubmed:author | pubmed-author:NemazeeDD | lld:pubmed |
| pubmed-article:9256471 | pubmed:author | pubmed-author:MelamedDD | lld:pubmed |
| pubmed-article:9256471 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9256471 | pubmed:day | 19 | lld:pubmed |
| pubmed-article:9256471 | pubmed:volume | 94 | lld:pubmed |
| pubmed-article:9256471 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9256471 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9256471 | pubmed:pagination | 9267-72 | lld:pubmed |
| pubmed-article:9256471 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:9256471 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:9256471 | pubmed:articleTitle | Self-antigen does not accelerate immature B cell apoptosis, but stimulates receptor editing as a consequence of developmental arrest. | lld:pubmed |
| pubmed-article:9256471 | pubmed:affiliation | Department of Pediatrics, Division of Basic Sciences, National Jewish Medical and Research Center, Denver, CO 80206, USA. | lld:pubmed |
| pubmed-article:9256471 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9256471 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:9256471 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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