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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

Molecular Immunology
|August 5, 2011
PubMed

Insights

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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