Linked Life Data

1913686

Source:http://linkedlifedata.com/resource/pubmed/id/1913686

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
20
pubmed:dateCreated
1991-11-13
pubmed:abstractText
Immune cytokines have been shown to play important roles in regulating immune cell functions as well as neoplastic cells. Interleukin-4 (IL4), primarily known as a B-cell growth factor, can also activate and differentiate other immune cells. This cytokine has recently been shown to have immunotherapeutic benefit in tumor-bearing hosts. The present study assessed the effect on human renal cell carcinoma cell lines of recombinant IL4 alone and in combination with recombinant gamma-interferon (IFN) or recombinant alpha-tumor necrosis factor (TNF). IL4 inhibited cell growth of all lines at 250-500 units/ml in a differential manner. Expression of IL4 receptors was demonstrated on renal cell carcinomas. Overall, IFN (500 units/ml) alone inhibited cell growth; however, TNF (500 units/ml) was not as strong an inhibitor. When IL4 was combined with IFN or TNF there was a significant augmentation of cell growth inhibition and modulation of cell morphology of the cell lines. Tumor-associated ganglioside antigens (NeuAc alpha 2-3Gal beta 1-4Glc beta 1-1'Cer, NeuAc alpha 2-8NeuAc alpha 2-3Gal beta 1-4Glc beta 1-1'Cer, GalNAc beta 1-4 (NeuAc alpha 2-3)Gal beta 1-4Glc beta 1-1'Cer, and GalNAc beta 1-4(NeuAc alpha 2-8NeuAc alpha 2-3)Gal beta 1-4Glc beta 1-1'Cer) HLA class I, HLA-DR, and beta 2-microglobulin on the cell surface of renal cancer lines were assessed by flow cytometry and radiometric binding assay. IL4 alone or in combination with other cytokines modulated HLA class I and HLA-DR expression. IL4 and IFN consistently enhanced NeuAc alpha 2-8NeuAc alpha 2-3Gal beta 1-4Glc beta 1-1'Cer and GalNAc beta 1-4(NeuAc alpha 2-8NeuAc alpha 2-3)Gal beta 1-4Glc beta 1-1'Cer expression on individual cell lines. The study demonstrated that IL4 alone or in combination with other cytokines can significantly inhibit growth, and modulate the expression of surface major histocompatibility and tumor-associated antigens of renal cell carcinomas.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
51
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5687-93
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:1913686-Carcinoma, Renal Cell, pubmed-meshheading:1913686-Cell Division, pubmed-meshheading:1913686-Dose-Response Relationship, Drug, pubmed-meshheading:1913686-Drug Screening Assays, Antitumor, pubmed-meshheading:1913686-Drug Synergism, pubmed-meshheading:1913686-Gangliosides, pubmed-meshheading:1913686-HLA-DR Antigens, pubmed-meshheading:1913686-Histocompatibility Antigens Class I, pubmed-meshheading:1913686-Humans, pubmed-meshheading:1913686-Interferon-gamma, pubmed-meshheading:1913686-Interleukin-4, pubmed-meshheading:1913686-Kidney Neoplasms, pubmed-meshheading:1913686-Receptors, Interleukin-4, pubmed-meshheading:1913686-Receptors, Mitogen, pubmed-meshheading:1913686-Recombinant Proteins, pubmed-meshheading:1913686-Tumor Necrosis Factor-alpha, pubmed-meshheading:1913686-beta 2-Microglobulin
pubmed:year
1991
pubmed:articleTitle
Interleukin 4 alone and with gamma-interferon or alpha-tumor necrosis factor inhibits cell growth and modulates cell surface antigens on human renal cell carcinomas.
pubmed:affiliation
John Wayne Cancer Institute, Santa Monica, California 90404.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't