The functional role of 55- and 75-kDa tumour necrosis factor receptors in human polymorphonuclear cells in vitro

Y Abe1, Y Osuka, T Nakata

  • 1Second Department of Surgery, Ehime University School of Medicine, Japan.

Cytokine
|January 1, 1995
PubMed

Insights

Human polymorphonuclear cells (PMN) primarily express tumour necrosis factor-receptor II (TNF-RII), but signalling of lymphotoxin (LT) and TNF primarily occurs via TNF-RI. This study investigates their distinct roles in PMN function.

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Tumour necrosis factor-receptors (TNF-R) mediate crucial cellular responses.
  • Polymorphonuclear cells (PMN) play a key role in inflammatory processes.
  • Understanding TNF-R function in PMN is vital for inflammatory disease research.

Purpose of the Study:

  • To elucidate the distinct roles of TNF-RI and TNF-RII in human PMN.
  • To investigate the signaling pathways of lymphotoxin (LT) and TNF in PMN.
  • To determine the impact of TNF-R activation on PMN functions like superoxide release, granule exocytosis, and adhesion.

Main Methods:

  • Utilized agonistic rabbit polyclonal anti-TNF-R antibodies to stimulate TNF-RI and TNF-RII.
  • Studied human PMN in vitro.
  • Assessed superoxide anion release, elastase and lactoferrin release, and Mac-1 expression.

Main Results:

  • PMN predominantly express TNF-RII, but LT/TNF signaling is mainly mediated by TNF-RI.
  • Anti-TNF-RI antibody stimulated superoxide release, elastase, and lactoferrin release, mimicking LT.
  • Anti-TNF-RI antibody upregulated PMN adhesiveness and Mac-1 expression; TNF-RII modulated adhesion when TNF-RI was stimulated.

Conclusions:

  • Human PMN primarily express TNF-RII, but TNF-RI mediates key LT/TNF signaling.
  • TNF-RI is the primary mediator of LT-induced superoxide release, granule exocytosis, and adhesion molecule upregulation in PMN.
  • TNF-RII plays a modulatory role in PMN adhesion, particularly in conjunction with TNF-RI activation.

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