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Intravenous immunoglobulin modulates human mononuclear phagocyte tumor necrosis factor-alpha production in vitro

T Darville1, D Tabor, K Simpson

  • 1Arkansas Children's Hospital, Little Rock 72202-3591.

Pediatric Research
|April 1, 1994
PubMed

Insights

Intravenous immunoglobulin (IgG) enhances tumor necrosis factor-alpha (TNF) production by monocytes when combined with inflammatory stimuli like LPS. This finding is relevant for treating neonatal sepsis and autoimmune diseases.

Area of Science:

  • Immunology
  • Cell Biology
  • Pharmacology

Background:

  • Mononuclear phagocytes (MO) produce tumor necrosis factor-alpha (TNF) in response to inflammatory stimuli, such as lipopolysaccharide (LPS).
  • Intravenous immunoglobulin (IgG) is being explored for treating neonatal sepsis and autoimmune disorders.
  • Fc receptor cross-linking on MO also triggers TNF release.

Purpose of the Study:

  • To investigate the in vitro effect of immunoglobulin-gamma (IgG) on TNF production by neonatal and adult mononuclear phagocytes (MO).
  • To determine if IgG alone or in combination with inflammatory stimuli influences TNF secretion.

Main Methods:

  • Mononuclear phagocytes (neonatal cord blood and adult) were incubated with varying concentrations of IgG (1-25 g/L) for different durations (2, 6, 24 hours).
  • Cells were either treated with IgG alone or preincubated with IgG followed by stimulation with interferon-gamma/lipopolysaccharide (LPS).
  • TNF secretion was quantified, and experiments included Fc, Fab, and F(ab')2 fragments to identify the active component.

Main Results:

  • IgG alone did not stimulate TNF secretion or production in MO.
  • Preincubation with IgG significantly enhanced TNF secretion when MO were subsequently stimulated with interferon-gamma/LPS.
  • This enhancement was observed in both neonatal and adult MO, with F(ab')2 fragments showing positive results, indicating the Fc region is not solely responsible.

Conclusions:

  • Immunoglobulin-gamma (IgG) does not induce TNF production independently but potentiates inflammatory responses in mononuclear phagocytes (MO).
  • The findings suggest a potential mechanism for IgG's therapeutic effects in inflammatory and infectious conditions.
  • Further research into the interaction of IgG fragments with MO is warranted.

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