pubmed-article:2143726 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:2143726 | lifeskim:mentions | umls-concept:C0330390 | lld:lifeskim |
pubmed-article:2143726 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:2143726 | lifeskim:mentions | umls-concept:C0024143 | lld:lifeskim |
pubmed-article:2143726 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
pubmed-article:2143726 | lifeskim:mentions | umls-concept:C0034790 | lld:lifeskim |
pubmed-article:2143726 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
pubmed-article:2143726 | lifeskim:mentions | umls-concept:C1171362 | lld:lifeskim |
pubmed-article:2143726 | lifeskim:mentions | umls-concept:C0020852 | lld:lifeskim |
pubmed-article:2143726 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:2143726 | lifeskim:mentions | umls-concept:C1515670 | lld:lifeskim |
pubmed-article:2143726 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:2143726 | pubmed:dateCreated | 1990-9-21 | lld:pubmed |
pubmed-article:2143726 | pubmed:abstractText | In the (SWR x NZB)F1 (SNF1) model of lupus nephritis, pathogenic variety of IgG anti-DNA autoantibodies are induced by certain T helper (Th) cells that are either CD4+ or CD4-CD8- (double negative; DN) in phenotype. From the spleens of eight SNF1 mice with lupus nephritis, 149 T cell lines were derived and out of these only 25 lines (approximately 17%) were capable of augmenting the production of pathogenic anti-DNA autoantibodies. Herein, we analyzed the T cell receptor (TcR) V beta genes used by 16 such pathogenic autoantibody-inducing Th cell lines. Twelve of the Th lines were CD4+ and among these five lines expressed V beta 8 (8.2 or 8.3). The V beta 8 gene family is contributed by the NZB parent to the SNF1 mice, since it is absent in the SWR parental strain. Three other CD4+ Th lines expressed V beta 4, another was V beta 2+ and one line with poor autoantibody-inducing capability expressed V beta 1. Four autoantibody-inducing Th lines from the SNF1 mice had a DN phenotype and these lines were also autoreactive, proliferating in response to syngeneic spleen cells. Among these DN Th lines, two expressed V beta 6 and one expressed V beta 8.1 TcR. Both of these are forbidden TcR directed against Mls-1a (Mlsa) autoantigens expressed by the SNF1 mice and such autoreactive T cells should have been deleted during thymic ontogeny. Thus, the DN Th cells of non-lpr SNF1 mice are different from the DN cells or MRL-lpr which lack helper activity and do not express forbidden TcR. The spleens of 6 out of 19 nephritic SNF1 animals tested also showed an expansion of forbidden autoreactive TcR+ cells that were mainly DN. Two of these animals expressed high levels of V beta 6 (anti-Mlsa) and V beta 11 (anti-I-E) TcR+ cells, three others had high levels of V beta 11+ cells alone and one animal had an expanded population of V beta 17a+ (anti-I-E) cells. The I-E-reactive TcR again should have been eliminated in the SNF1 thymus, since they express I-E molecules contributed by the NZB parent. The SWR parents of SNF1, are I-E-; moreover, they lack the V beta 11 gene but they express V beta 17a in peripheral T cells. Whereas the NZB parents are I-E+, they lack a functional V beta 17a gene and they delete mature V beta 11+ T cells.(ABSTRACT TRUNCATED AT 250 WORDS) | lld:pubmed |
pubmed-article:2143726 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2143726 | pubmed:language | eng | lld:pubmed |
pubmed-article:2143726 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2143726 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:2143726 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2143726 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2143726 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2143726 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2143726 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:2143726 | pubmed:month | Jul | lld:pubmed |
pubmed-article:2143726 | pubmed:issn | 0014-2980 | lld:pubmed |
pubmed-article:2143726 | pubmed:author | pubmed-author:DattaSS | lld:pubmed |
pubmed-article:2143726 | pubmed:author | pubmed-author:AdamsSS | lld:pubmed |
pubmed-article:2143726 | pubmed:author | pubmed-author:SainisKK | lld:pubmed |
pubmed-article:2143726 | pubmed:author | pubmed-author:ZordanTT | lld:pubmed |
pubmed-article:2143726 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:2143726 | pubmed:volume | 20 | lld:pubmed |
pubmed-article:2143726 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:2143726 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:2143726 | pubmed:pagination | 1435-43 | lld:pubmed |
pubmed-article:2143726 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:2143726 | pubmed:year | 1990 | lld:pubmed |
pubmed-article:2143726 | pubmed:articleTitle | T cell receptor V beta genes expressed by IgG anti-DNA autoantibody-inducing T cells in lupus nephritis: forbidden receptors and double-negative T cells. | lld:pubmed |
pubmed-article:2143726 | pubmed:affiliation | Department of Medicine, New England Medical Center, Boston, MA 02111. | lld:pubmed |
pubmed-article:2143726 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:2143726 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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