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Tumour necrosis factor triggers granulocytes to internalize complement-coated virus particles
J A van Strijp1, M E van der Tol, L A Miltenburg
1Eijkman-Winkler Laboratory of Medical Microbiology, Utrecht University, The Netherlands.
Immunology
|May 1, 1991
Summary
Tumor necrosis factor-alpha (TNF-alpha) enhances human polymorphonuclear leucocytes (PMN) ability to internalize herpes simplex virus (HSV). This discovery reveals a novel non-specific defense mechanism against HSV infection.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Monocytes produce tumor necrosis factor-alpha (TNF-alpha) when encountering herpes simplex virus (HSV).
- TNF-alpha's role in regulating anti-viral functions of human polymorphonuclear leucocytes (PMN) requires further investigation.
Purpose of the Study:
- To investigate the effect of TNF-alpha on human PMN's anti-viral functions against HSV.
- To explore the mechanism of HSV internalization by PMN.
Main Methods:
- Flow cytometric analysis was used to monitor the uptake of fluorescein-labeled HSV by human PMN.
- Human PMN were primed with recombinant human TNF-alpha and granulocyte-macrophage colony-stimulating factor (GM-CSF) to assess their effects on HSV internalization and anti-viral defense parameters.
Main Results:
- Priming with TNF-alpha induced complement receptor-mediated internalization of complement-coated HSV by human PMN, a novel observation.
- Both TNF-alpha and GM-CSF enhanced PMN respiratory burst and membrane potential depolarization when triggered by HSV-containing immune complexes.
- While both cytokines enhanced HSV uptake in the presence of antibody and/or complement, they did not affect the processing of phagocytosed HSV.
Conclusions:
- TNF-alpha and GM-CSF effectively modulate PMN to enhance virus removal, particularly in inflammatory settings.
- TNF-alpha, in conjunction with PMN and complement, represents a potential novel non-specific defense mechanism against HSV.