| pubmed-article:2430283 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2430283 | lifeskim:mentions | umls-concept:C0025936 | lld:lifeskim |
| pubmed-article:2430283 | lifeskim:mentions | umls-concept:C0031437 | lld:lifeskim |
| pubmed-article:2430283 | lifeskim:mentions | umls-concept:C2003941 | lld:lifeskim |
| pubmed-article:2430283 | lifeskim:mentions | umls-concept:C0205349 | lld:lifeskim |
| pubmed-article:2430283 | pubmed:issue | 21 | lld:pubmed |
| pubmed-article:2430283 | pubmed:dateCreated | 1986-12-5 | lld:pubmed |
| pubmed-article:2430283 | pubmed:abstractText | One of the more intriguing puzzles in immunology is the genetic basis for control of murine T-cell I-J determinants. Molecules bearing I-J determinants (I-J molecules) play a role in information trafficking among immunocompetent cells, probably serving as self-recognition molecules that channel regulatory factors to their appropriate target cells. Although it is clear that I-J polymorphism is influenced by the major histocompatibility complex (MHC), molecular genetic studies provide evidence that an MHC gene does not encode I-J molecules. A possible explanation for this paradox is that I-J molecules are a set of non-MHC-encoded T cell receptors that are directly or indirectly selected for by self-MHC products. One key to resolving the genetic and molecular basis for control of I-J determinants is the identification of the MHC gene(s) involved. Herein, data are presented which show that E alpha transgenic mice express an altered I-J phenotype, providing clear evidence that I region class II genes influence I-J polymorphism. Although further study is required to resolve how class II genes mediate this effect, this is a major piece to the I-J puzzle. | lld:pubmed |
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| pubmed-article:2430283 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2430283 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2430283 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:2430283 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2430283 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:2430283 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:2430283 | pubmed:author | pubmed-author:MurphyD BDB | lld:pubmed |
| pubmed-article:2430283 | pubmed:author | pubmed-author:BenoistCC | lld:pubmed |
| pubmed-article:2430283 | pubmed:author | pubmed-author:MathisDD | lld:pubmed |
| pubmed-article:2430283 | pubmed:author | pubmed-author:FloodP MPM | lld:pubmed |
| pubmed-article:2430283 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2430283 | pubmed:volume | 83 | lld:pubmed |
| pubmed-article:2430283 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2430283 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2430283 | pubmed:pagination | 8308-12 | lld:pubmed |
| pubmed-article:2430283 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:2430283 | pubmed:meshHeading | pubmed-meshheading:2430283-... | lld:pubmed |
| pubmed-article:2430283 | pubmed:year | 1986 | lld:pubmed |
| pubmed-article:2430283 | pubmed:articleTitle | Altered I-J phenotype in E alpha transgenic mice. | lld:pubmed |
| pubmed-article:2430283 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2430283 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:2430283 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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