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Recombinant human tumor necrosis factor increases granulocyte cell-surface complement receptor number
1Department of Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.
Exposure of human buffy-coat granulocytes to tumor necrosis factor (TNF) produced cellular activation as indicated by an increase in the neutrophil and monocyte cell-surface number of C3b receptors (measured by indirect immunofluorescence). The degree of receptor increase depended on the dose of TNF from 25 to 1250 pg/mL. Results of kinetic analysis confirmed this response: TNF, 250 pg/mL, caused an increase in the C3b receptor number within ten minutes. Purified neutrophils exhibited a similar increase in cell-surface C3b receptors dependent on the concentration of TNF. Tumor necrosis factor could be a mediator of granulocyte activation in patients.
Exposure of human buffy-coat granulocytes to tumor necrosis factor (TNF) produced cellular activation as indicated by an increase in the neutrophil and monocyte cell-surface number of C3b receptors (measured by indirect immunofluorescence). The degree of receptor increase depended on the dose of TNF from 25 to 1250 pg/mL. Results of kinetic analysis confirmed this response: TNF, 250 pg/mL, caused an increase in the C3b receptor number within ten minutes. Purified neutrophils exhibited a similar increase in cell-surface C3b receptors dependent on the concentration of TNF. Tumor necrosis factor could be a mediator of granulocyte activation in patients.