TUMOR-NECROSIS-FACTOR-ALPHA AND SOLUBLE TUMOR-NECROSIS-FACTOR RECEPTORS IN THE CULTURE SUPERNATANTS OF POLYMORPHONUCLEAR CELLS AND PERIPHERAL-BLOOD MONONUCLEAR-CELLS FROM CANCER-PATIENTS

Citation
E. Jablonska et al., TUMOR-NECROSIS-FACTOR-ALPHA AND SOLUBLE TUMOR-NECROSIS-FACTOR RECEPTORS IN THE CULTURE SUPERNATANTS OF POLYMORPHONUCLEAR CELLS AND PERIPHERAL-BLOOD MONONUCLEAR-CELLS FROM CANCER-PATIENTS, European cytokine network, 9(2), 1998, pp. 155-159
Citations number
18
Categorie Soggetti
Immunology,Biology,"Cell Biology
Journal title
ISSN journal
11485493
Volume
9
Issue
2
Year of publication
1998
Pages
155 - 159
Database
ISI
SICI code
1148-5493(1998)9:2<155:TASTR>2.0.ZU;2-E
Abstract
Recent clinical and experimental studies have focused on the measureme nt of cytokines and their regulators, produced by immunocompetent cell s. Their estimation may be used as parameters for the immune potential of cancer patients. In the present study we studied the ability of un stimulated and lipopolysaccharide (LPS)-stimulated polymorphonuclear c ells (PMN) and peripheral blood mononuclear cells (PBMC) from oral cav ity cancer and breast cancer patients to release tumor necrosis factor alpha (TNF-alpha) and soluble tumor necrosis factor receptors (sTNFR) , There were significant differences concerning the parameters examine d for PMN and PBMC from cancer patients as compared with normal subjec ts. We found significantly higher concentrations of sTNFR p75 than sTN F-R p55 in the cell-culture supernatants. The culture supernatants of cells from oral cavity cancer patients contained higher concentrations of TNF-alpha and lower concentrations of sTNF-R p55 and sTNF-R p75 in comparison with breast cancer cell supernatants. In contrast, cells f rom breast cancer patients secreted lower concentrations of TNF-alpha and higher concentrations of sTNF-R p55 and sTNF-R p75. Although PBMC secreted higher concentrations of mediators than PMN, the quantitative dominance of PMN in the peripheral blood suggests an essential role o f these cells in the defense reactions controlled by TNF-alpha.