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Recombinant human tumor necrosis factor increases granulocyte cell-surface complement receptor number.

D Reed1, F D Moore

  • 1Department of Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.

Archives of Surgery (Chicago, Ill. : 1960)
|November 1, 1988
PubMed
Summary

Tumor necrosis factor (TNF) activates human granulocytes, increasing C3b receptors on neutrophils and monocytes. This cellular activation is dose- and time-dependent, suggesting TNF

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Area of Science:

  • Immunology
  • Cell Biology
  • Inflammation Research

Background:

  • Granulocytes play a crucial role in the immune response.
  • Cellular activation is a key process in immune cell function.
  • Tumor necrosis factor (TNF) is a pro-inflammatory cytokine involved in various biological processes.

Purpose of the Study:

  • To investigate the effect of tumor necrosis factor (TNF) on human granulocyte activation.
  • To quantify the changes in C3b receptor expression on granulocytes upon TNF exposure.
  • To determine the dose- and time-dependency of TNF-induced granulocyte activation.

Main Methods:

  • Human buffy-coat granulocytes were exposed to varying concentrations of TNF.
  • Cell-surface C3b receptor expression was measured using indirect immunofluorescence.

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  • Kinetic analysis was performed to assess the time course of the response.
  • Purified neutrophils were also utilized to confirm findings.

    • Main Results:

    • TNF exposure led to a dose-dependent increase in C3b receptors on neutrophils and monocytes.
    • A significant increase in C3b receptors was observed within 10 minutes of TNF stimulation (250 pg/mL).
    • Purified neutrophils showed a similar TNF-induced upregulation of C3b receptors.

    Conclusions:

    • Tumor necrosis factor (TNF) effectively activates human granulocytes.
    • TNF significantly enhances the expression of C3b receptors on neutrophils and monocytes.
    • These findings suggest that TNF may act as a mediator of granulocyte activation in patients.