pubmed-article:8253530 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:8253530 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:8253530 | lifeskim:mentions | umls-concept:C1155065 | lld:lifeskim |
pubmed-article:8253530 | lifeskim:mentions | umls-concept:C0431085 | lld:lifeskim |
pubmed-article:8253530 | lifeskim:mentions | umls-concept:C0108779 | lld:lifeskim |
pubmed-article:8253530 | lifeskim:mentions | umls-concept:C0206491 | lld:lifeskim |
pubmed-article:8253530 | lifeskim:mentions | umls-concept:C0599894 | lld:lifeskim |
pubmed-article:8253530 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
pubmed-article:8253530 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:8253530 | pubmed:dateCreated | 1994-1-10 | lld:pubmed |
pubmed-article:8253530 | pubmed:abstractText | Targeting of T lymphocytes against epidermal growth-factor-receptor (EGF-R)+ tumor cells was achieved by constructing a hybrid hybridoma which secretes an anti-EGF-R/anti-CD3 bispecific monoclonal antibody (biMAb) of hybrid isotype (IgG1/IgG2a). Purification of biMAb molecules from parental anti-EGF-R and anti-CD3 MAbs was performed by protein-A chromatography. The purified biMAb was able to trigger the lysis of EGF-R+ tumor cell lines (A431, IGROV-1, MDA-468 and U-87) and of NIH-3T3 transfectants expressing human EGF-R by cytolytic T lymphocytes, but it was ineffective in the case of EGF-R-negative tumor targets. Normal EGF-R+ cells (keratinocytes and endometrial cells) were also susceptible to biMAb-targeted cytolysis. However, the amount of biMAb required to induce half-maximal cytolysis of tumor cells over-expressing the EGF-R molecule (A431) was considerably lower than that required to induce lysis of EGF-R+ tumor or normal cells which express EGF-R at considerably lower density. The ability of such biMAbs to deliver activation signals to T cells was evaluated by Ca++ mobilization and lymphokine production experiments. The soluble anti-EGF-R/anti-CD3 biMAb failed to induce intracellular Ca++ increases, which occurred only after cross-linking induced by an anti-mouse IgG antibody. Secretion of lymphokines (IFN-gamma, TNF-alpha and GM-CSF) was induced by contact of the biMAb-coated effector cells with the relevant tumor target, whereas the soluble biMAb was virtually ineffective. In addition, biMAb-coated effector cells retained the ability to recognize and to lyse EGF-R+ tumor cells for a prolonged period of time. Our data indicate that activation of effector cells targeted by biMAbs can only occur at the tumor site, where cross-linking of surface CD3 molecules is induced by contact with the tumor cells. | lld:pubmed |
pubmed-article:8253530 | pubmed:language | eng | lld:pubmed |
pubmed-article:8253530 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8253530 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:8253530 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8253530 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8253530 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8253530 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8253530 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8253530 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:8253530 | pubmed:month | Dec | lld:pubmed |
pubmed-article:8253530 | pubmed:issn | 0020-7136 | lld:pubmed |
pubmed-article:8253530 | pubmed:author | pubmed-author:CanevariSS | lld:pubmed |
pubmed-article:8253530 | pubmed:author | pubmed-author:MorettaLL | lld:pubmed |
pubmed-article:8253530 | pubmed:author | pubmed-author:ColnaghiM IMI | lld:pubmed |
pubmed-article:8253530 | pubmed:author | pubmed-author:GrossiC ECE | lld:pubmed |
pubmed-article:8253530 | pubmed:author | pubmed-author:SforziniSS | lld:pubmed |
pubmed-article:8253530 | pubmed:author | pubmed-author:FerriniSS | lld:pubmed |
pubmed-article:8253530 | pubmed:author | pubmed-author:CambiaggiAA | lld:pubmed |
pubmed-article:8253530 | pubmed:author | pubmed-author:MezzanzanicaD... | lld:pubmed |
pubmed-article:8253530 | pubmed:author | pubmed-author:MarcianoSS | lld:pubmed |
pubmed-article:8253530 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:8253530 | pubmed:day | 2 | lld:pubmed |
pubmed-article:8253530 | pubmed:volume | 55 | lld:pubmed |
pubmed-article:8253530 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:8253530 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:8253530 | pubmed:pagination | 931-7 | lld:pubmed |
pubmed-article:8253530 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:8253530 | pubmed:year | 1993 | lld:pubmed |
pubmed-article:8253530 | pubmed:articleTitle | Targeting of T lymphocytes against EGF-receptor+ tumor cells by bispecific monoclonal antibodies: requirement of CD3 molecule cross-linking for T-cell activation. | lld:pubmed |
pubmed-article:8253530 | pubmed:affiliation | Istituto Nazionale per la Ricerca sul Cancro, Genoa, Italy. | lld:pubmed |
pubmed-article:8253530 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:8253530 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:8253530 | lld:pubmed |