| pubmed-article:1831490 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1831490 | lifeskim:mentions | umls-concept:C0332307 | lld:lifeskim |
| pubmed-article:1831490 | lifeskim:mentions | umls-concept:C0006034 | lld:lifeskim |
| pubmed-article:1831490 | lifeskim:mentions | umls-concept:C2362651 | lld:lifeskim |
| pubmed-article:1831490 | lifeskim:mentions | umls-concept:C0242381 | lld:lifeskim |
| pubmed-article:1831490 | lifeskim:mentions | umls-concept:C1515877 | lld:lifeskim |
| pubmed-article:1831490 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:1831490 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:1831490 | pubmed:dateCreated | 1991-9-26 | lld:pubmed |
| pubmed-article:1831490 | pubmed:abstractText | 18 cloned T cell lines reactive with Borrelia burgdorferi proteins, all CD3+4+8-TCR-alpha/beta+ and restricted by HLA class II proteins, were isolated from four patients with chronic Lyme arthritis. Analysis of these T cell clones indicated that the T cell response to the Lyme disease spirochete is not oligoclonally restricted; yet all produced the same pattern of lymphokines, resembling that of murine type 1 T helper cells, after antigen-specific or nonspecific stimulation. Therefore, a subset of human CD4+ T cells, with a distinct profile of lymphokine secretion, is selectively activated by the pathogen inciting this chronic inflammatory disease. | lld:pubmed |
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| pubmed-article:1831490 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:1831490 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1831490 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1831490 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:1831490 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:1831490 | pubmed:author | pubmed-author:YsselHH | lld:pubmed |
| pubmed-article:1831490 | pubmed:author | pubmed-author:PeltzGG | lld:pubmed |
| pubmed-article:1831490 | pubmed:author | pubmed-author:SoderbergCC | lld:pubmed |
| pubmed-article:1831490 | pubmed:author | pubmed-author:ShanafeltM... | lld:pubmed |
| pubmed-article:1831490 | pubmed:author | pubmed-author:AnzolaJJ | lld:pubmed |
| pubmed-article:1831490 | pubmed:author | pubmed-author:SchneiderP... | lld:pubmed |
| pubmed-article:1831490 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1831490 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:1831490 | pubmed:volume | 174 | lld:pubmed |
| pubmed-article:1831490 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1831490 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1831490 | pubmed:pagination | 593-601 | lld:pubmed |
| pubmed-article:1831490 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:1831490 | pubmed:year | 1991 | lld:pubmed |
| pubmed-article:1831490 | pubmed:articleTitle | Borrelia burgdorferi activates a T helper type 1-like T cell subset in Lyme arthritis. | lld:pubmed |
| pubmed-article:1831490 | pubmed:affiliation | Department of Inflammation Biology, Syntex Research, Palo Alto, California 94303. | lld:pubmed |
| pubmed-article:1831490 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1831490 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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