| pubmed-article:3258351 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:3258351 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:3258351 | lifeskim:mentions | umls-concept:C0205102 | lld:lifeskim |
| pubmed-article:3258351 | lifeskim:mentions | umls-concept:C0015127 | lld:lifeskim |
| pubmed-article:3258351 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
| pubmed-article:3258351 | lifeskim:mentions | umls-concept:C1314792 | lld:lifeskim |
| pubmed-article:3258351 | lifeskim:mentions | umls-concept:C1704258 | lld:lifeskim |
| pubmed-article:3258351 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:3258351 | lifeskim:mentions | umls-concept:C1556066 | lld:lifeskim |
| pubmed-article:3258351 | lifeskim:mentions | umls-concept:C1619636 | lld:lifeskim |
| pubmed-article:3258351 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
| pubmed-article:3258351 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:3258351 | pubmed:dateCreated | 1988-5-2 | lld:pubmed |
| pubmed-article:3258351 | pubmed:abstractText | The lpr gene induces marked lymphoproliferation characterized by the massive accumulation of T cells of an unusual phenotype and concomitant autoimmune disease. To clarify the mechanism of the lpr effect, bone marrow cells from B6-lpr/lpr (Ly-1.2) and B6-+/+ (Ly-1.1) mice were transferred into lethally irradiated B6-lpr/lpr mice. As has been previously reported, recipients of the B6-lpr/lpr bone marrow showed the typical lpr phenotype with marked lymphadenopathy, splenomegaly and increased levels of autoantibodies; while the recipients of B6-+/+ bone marrow had normal sized lymph nodes and spleen and no autoantibodies. A third group of mice received an equal mixture of bone marrow cells from the B6-lpr/lpr and B6-+/+ donors. These mice showed both lymphadenopathy and autoantibody production comparable to that of recipients of the B6-lpr/lpr marrow alone. Immunofluorocytometric analysis of the lymphoid populations in these mixed bone marrow recipients established that the T cells from the lpr/lpr and +/+ donors were equivalently represented in the peripheral blood and thymus. In striking contrast, the T cells that accumulated in abnormally large numbers in the lymph nodes were almost entirely from the lpr donor. Their surface phenotype was Thy-1+(dull), Ly-1.2+(dull), Lyt-2-, L3T4-, 9F3+, and 3A1+, which is consistent with that found in intact lpr mice. These results indicate that the lpr gene causes an intrinsic defect directly within the T cells that accumulate in large numbers in lpr mice. In addition, the presence of the +/+ T cells cannot prevent the expression of the lpr abnormalities. | lld:pubmed |
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| pubmed-article:3258351 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:3258351 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:3258351 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:3258351 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:3258351 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:3258351 | pubmed:author | pubmed-author:KatagiriTT | lld:pubmed |
| pubmed-article:3258351 | pubmed:author | pubmed-author:CohenP LPL | lld:pubmed |
| pubmed-article:3258351 | pubmed:author | pubmed-author:EisenbergR... | lld:pubmed |
| pubmed-article:3258351 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:3258351 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:3258351 | pubmed:volume | 167 | lld:pubmed |
| pubmed-article:3258351 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:3258351 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:3258351 | pubmed:pagination | 741-51 | lld:pubmed |
| pubmed-article:3258351 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:3258351 | pubmed:year | 1988 | lld:pubmed |
| pubmed-article:3258351 | pubmed:articleTitle | The lpr gene causes an intrinsic T cell abnormality that is required for hyperproliferation. | lld:pubmed |
| pubmed-article:3258351 | pubmed:affiliation | Department of Medicine, University of North Carolina, Chapel Hill 27599. | lld:pubmed |
| pubmed-article:3258351 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:3258351 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:3258351 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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