| pubmed-article:1716521 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1716521 | lifeskim:mentions | umls-concept:C0035647 | lld:lifeskim |
| pubmed-article:1716521 | lifeskim:mentions | umls-concept:C0026473 | lld:lifeskim |
| pubmed-article:1716521 | lifeskim:mentions | umls-concept:C0021745 | lld:lifeskim |
| pubmed-article:1716521 | lifeskim:mentions | umls-concept:C1155065 | lld:lifeskim |
| pubmed-article:1716521 | lifeskim:mentions | umls-concept:C1332709 | lld:lifeskim |
| pubmed-article:1716521 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:1716521 | lifeskim:mentions | umls-concept:C1948023 | lld:lifeskim |
| pubmed-article:1716521 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:1716521 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:1716521 | lifeskim:mentions | umls-concept:C1521871 | lld:lifeskim |
| pubmed-article:1716521 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:1716521 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:1716521 | pubmed:dateCreated | 1991-10-22 | lld:pubmed |
| pubmed-article:1716521 | pubmed:abstractText | The B cell activation antigen B7/BB-1 is the natural ligand for the T cell antigen CD28 and these two molecules are capable of mediating T-B cell adhesion. Engagement of the CD28 pathway provides a costimulatory signal to T cells leading to enhanced lymphokine production. We report that interferon-gamma (INF-gamma) induces the expression of B7/BB-1 on monocytes. This induction was very specific since other cytokines and stimuli which activate monocytes including M-CSF, GM-CSF, IL3, TNF-alpha, and LPS were unable to induce B7/BB-1. Following culture of monocytes with INF-gamma, maximal mRNA and cell surface B7/BB-1 expression was detected at 12 and 24 hr, respectively. In addition to antigen presentation, optimal T cell activation and lymphokine synthesis require an additional cell to cell contact signal provided by the antigen presenting cell. The induction of B7/BB-1 on monocytes and subsequent heterophilic interaction of B7/BB-1 with CD28 may provide a mechanism for the amplification of T cell proliferation and lymphokine production by INF-gamma activated monocytes. | lld:pubmed |
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| pubmed-article:1716521 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:1716521 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1716521 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1716521 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:1716521 | pubmed:issn | 0008-8749 | lld:pubmed |
| pubmed-article:1716521 | pubmed:author | pubmed-author:NadlerL MLM | lld:pubmed |
| pubmed-article:1716521 | pubmed:author | pubmed-author:FreemanG JGJ | lld:pubmed |
| pubmed-article:1716521 | pubmed:author | pubmed-author:FreedmanA SAS | lld:pubmed |
| pubmed-article:1716521 | pubmed:author | pubmed-author:RhynhartKK | lld:pubmed |
| pubmed-article:1716521 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1716521 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:1716521 | pubmed:volume | 137 | lld:pubmed |
| pubmed-article:1716521 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1716521 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1716521 | pubmed:pagination | 429-37 | lld:pubmed |
| pubmed-article:1716521 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:1716521 | pubmed:year | 1991 | lld:pubmed |
| pubmed-article:1716521 | pubmed:articleTitle | Selective induction of B7/BB-1 on interferon-gamma stimulated monocytes: a potential mechanism for amplification of T cell activation through the CD28 pathway. | lld:pubmed |
| pubmed-article:1716521 | pubmed:affiliation | Division of Tumor Immunology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115. | lld:pubmed |
| pubmed-article:1716521 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1716521 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:1716521 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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