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Updated: May 30, 2026

Isolation and Characterization of Neutrophils with Anti-Tumor Properties
Published on: June 19, 2015
Neutrophils and T cells: bidirectional effects and functional interferences.
Marielle Thewissen1, Jan Damoiseaux, Jose van de Gaar
1Department of Internal Medicine, Clinical and Experimental Immunology, Maastricht University Medical Center+, PO Box 616, 6200 MD Maastricht, The Netherlands. marielle.thewissen@maastrichtuniversity.nl
Polymorphonuclear cells (PMN) suppress T cell activation and viability through contact-dependent mechanisms. Arginase and calprotectin are involved, influencing T cell proliferation and cytokine production.
Area of Science:
- Immunology
- Cell Biology
Background:
- Polymorphonuclear cells (PMN) are key immune cells involved in microbial infections.
- Recent research highlights PMN's functional interactions with other immune cells.
- Understanding PMN-T cell cross-talk is crucial for immune response regulation.
Purpose of the Study:
- To investigate the in vitro interactions between PMN and T cells.
- To elucidate the mechanisms by which PMN influence T cell function.
- To identify specific molecules involved in PMN-T cell cross-talk.
Main Methods:
- In vitro co-culture of PMN and T cells.
- Flow cytometry to assess CD66b expression and T cell activation markers.
- Transwell co-culture system to differentiate contact-dependent effects.
- Treatment with arginase-inhibitor and blocking antibodies (anti-calprotectin, anti-MPO).
Main Results:
- PMN presence impaired anti-CD3 induced CD4(+) T cell activation, proliferation, and viability in a dose-dependent manner.
- Suppression was contact-dependent, as T cell proliferation increased in transwell co-cultures.
- Arginase inhibition and anti-calprotectin antibodies partially restored T cell proliferation.
- PMN altered T cell cytokine profiles, increasing IFN-γ and IL-17, and decreasing IL-10 production.
Conclusions:
- PMN and T cells engage in significant cross-talk, impacting T cell function.
- Contact-dependent mechanisms mediated by PMN suppress T cell responses under non-inflammatory conditions.
- Arginase and calprotectin are key mediators in PMN-induced T cell modulation.
- Further research is needed to explore PMN-T cell interactions in inflammatory settings.
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