Linked Life Data

8144194

Source:http://linkedlifedata.com/resource/pubmed/id/8144194

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1994-5-2
pubmed:abstractText
Functional characteristics were established for a genetically engineered fusion protein between human IL2 and mouse/human chimeric mAb 225 directed against human epidermal growth factor receptor (EGFR), aberrantly expressed on human melanoma cells. The emphasis of these studies was on the mechanism(s) of action by which the ch225-IL2 fusion protein mediated cytotoxic killing of human melanoma cells by different human immune effector cells. Ch225-IL2 fusion protein bound to human EGFR with the high affinity of the parental antibody, and was as active as the equivalent amount of rhIL2. Ch225-IL2 enhanced cellular cytotoxicity mediated by freshly separated PBMC, isolated natural killer (NK) cells and activated T cells against melanoma cell lines. NK cells, which constitutively express both Fc gamma RIII and IL2R, interacted with ch225-IL2, mainly through Fc gamma RIII, while the involvement of IL2R was secondary. However, the effect of ch225-IL2 on activated T cells was most likely mediated through IL2R. These results suggest that the genetically engineered ch225-IL2 fusion protein may become a potent immunotherapeutic agent capable of stimulating various immune effector populations to effectively kill human melanoma cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0165-2478
pubmed:author
pubmed:issnType
Print
pubmed:volume
39
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
91-9
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Mechanisms of cellular cytotoxicity mediated by a recombinant antibody-IL2 fusion protein against human melanoma cells.
pubmed:affiliation
Scripps Research Institute, La Jolla, CA 92037.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.