| pubmed-article:1645270 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1645270 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:1645270 | lifeskim:mentions | umls-concept:C0104998 | lld:lifeskim |
| pubmed-article:1645270 | lifeskim:mentions | umls-concept:C1704675 | lld:lifeskim |
| pubmed-article:1645270 | lifeskim:mentions | umls-concept:C1332709 | lld:lifeskim |
| pubmed-article:1645270 | lifeskim:mentions | umls-concept:C0439851 | lld:lifeskim |
| pubmed-article:1645270 | lifeskim:mentions | umls-concept:C1155004 | lld:lifeskim |
| pubmed-article:1645270 | lifeskim:mentions | umls-concept:C1552596 | lld:lifeskim |
| pubmed-article:1645270 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:1645270 | lifeskim:mentions | umls-concept:C1947931 | lld:lifeskim |
| pubmed-article:1645270 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:1645270 | pubmed:dateCreated | 1991-6-28 | lld:pubmed |
| pubmed-article:1645270 | pubmed:abstractText | Cognate interactions between major histocompatibility complex class II antigen (Ag)-reactive CD4+ T helper (Th) and Ag-presenting B cells induce first the activation of B cells and their subsequent differentiation into Ig-secreting cells (IgSC). The Th cell-associated homodimeric glycoprotein CD28 has been implicated as an important regulator of Th activation. Recently, B cell-associated early activation Ag B7 has been identified as a ligand for the CD28 molecule. In this study, we have examined using monoclonal antibodies (mAb) the roles of CD28 and B7 molecules during the Th-B cell cognate interactions leading to the differentiation of B7+ B cells. Anti-CD28 mAb 9.3 specifically inhibited proliferative responses of CD4+ T cells to both allogeneic B cells and soluble Ag-presenting autologous non-T cells. In addition, anti-CD28 mAb 9.3 inhibited Th-induced differentiation of alloantigen-presenting B cells into ISC. Similar inhibition of both Ag-induced Th activation and B cell differentiation into ISC was observed using mAb BB1 which recognizes a B cell-associated molecule B7. In contrast, non-cognate Th-independent exogenous interleukin 6-induced differentiation of B7+ B cells into ISC was not inhibited by mAb to either molecule. These results clearly demonstrate the involvement of CD28 on Th and its ligand B7 on B cells during cognate Th-B interactions leading to the differentiation of B cells. Furthermore, these results also suggest the development of new mAb-based therapeutic approaches for exaggerated B cell activation associated with certain autoimmune diseases such as systemic lupus erythematosus. | lld:pubmed |
| pubmed-article:1645270 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1645270 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1645270 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:1645270 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1645270 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1645270 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1645270 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1645270 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1645270 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1645270 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1645270 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1645270 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1645270 | pubmed:month | May | lld:pubmed |
| pubmed-article:1645270 | pubmed:issn | 0014-2980 | lld:pubmed |
| pubmed-article:1645270 | pubmed:author | pubmed-author:LinsleyP SPS | lld:pubmed |
| pubmed-article:1645270 | pubmed:author | pubmed-author:DamleN KNK | lld:pubmed |
| pubmed-article:1645270 | pubmed:author | pubmed-author:LedbetterJ... | lld:pubmed |
| pubmed-article:1645270 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1645270 | pubmed:volume | 21 | lld:pubmed |
| pubmed-article:1645270 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1645270 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1645270 | pubmed:pagination | 1277-82 | lld:pubmed |
| pubmed-article:1645270 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
| pubmed-article:1645270 | pubmed:meshHeading | pubmed-meshheading:1645270-... | lld:pubmed |
| pubmed-article:1645270 | pubmed:meshHeading | pubmed-meshheading:1645270-... | lld:pubmed |
| pubmed-article:1645270 | pubmed:meshHeading | pubmed-meshheading:1645270-... | lld:pubmed |
| pubmed-article:1645270 | pubmed:meshHeading | pubmed-meshheading:1645270-... | lld:pubmed |
| pubmed-article:1645270 | pubmed:meshHeading | pubmed-meshheading:1645270-... | lld:pubmed |
| pubmed-article:1645270 | pubmed:meshHeading | pubmed-meshheading:1645270-... | lld:pubmed |
| pubmed-article:1645270 | pubmed:meshHeading | pubmed-meshheading:1645270-... | lld:pubmed |
| pubmed-article:1645270 | pubmed:meshHeading | pubmed-meshheading:1645270-... | lld:pubmed |
| pubmed-article:1645270 | pubmed:meshHeading | pubmed-meshheading:1645270-... | lld:pubmed |
| pubmed-article:1645270 | pubmed:meshHeading | pubmed-meshheading:1645270-... | lld:pubmed |
| pubmed-article:1645270 | pubmed:meshHeading | pubmed-meshheading:1645270-... | lld:pubmed |
| pubmed-article:1645270 | pubmed:meshHeading | pubmed-meshheading:1645270-... | lld:pubmed |
| pubmed-article:1645270 | pubmed:meshHeading | pubmed-meshheading:1645270-... | lld:pubmed |
| pubmed-article:1645270 | pubmed:meshHeading | pubmed-meshheading:1645270-... | lld:pubmed |
| pubmed-article:1645270 | pubmed:meshHeading | pubmed-meshheading:1645270-... | lld:pubmed |
| pubmed-article:1645270 | pubmed:year | 1991 | lld:pubmed |
| pubmed-article:1645270 | pubmed:articleTitle | Direct helper T cell-induced B cell differentiation involves interaction between T cell antigen CD28 and B cell activation antigen B7. | lld:pubmed |
| pubmed-article:1645270 | pubmed:affiliation | Oncogen Division, Bristol-Myers Squibb Pharmaceutical Research Institute, Seattle, WA 98121. | lld:pubmed |
| pubmed-article:1645270 | pubmed:publicationType | Journal Article | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:1645270 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:1645270 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:1645270 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:1645270 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:1645270 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:1645270 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:1645270 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:1645270 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:1645270 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:1645270 | lld:pubmed |
