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Phenotypic and functional changes of GM-CSF differentiated human macrophages following exposure to apoptotic

Elena R Chernykh1, Ludmila V Sakhno1, Ekaterina Ya Shevela1

  • 1Federal State Budget Scientific Institute «The Research Institute of Fundamental and Clinical Immunology», Yadrintsevskaya Street, 14, Novosibirsk 630099, Russian Federation.

Cellular Immunology
|June 14, 2018
PubMed

Insights

Engulfing apoptotic neutrophils induces M2 polarization in human macrophages (GM-Mφ). These M2 macrophages (GM-MφNeu) suppress T-cell proliferation via enhanced prostaglandin E2 (PGE2) synthesis, not IL-10.

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Monocyte and macrophage engulfment of apoptotic cells typically leads to M2 polarization.
  • Human macrophages differentiated with granulocyte-macrophage colony-stimulating factor (GM-CSF) are termed GM-Mφ.

Purpose of the Study:

  • To investigate the impact of apoptotic cells on the phenotype and function of GM-Mφ.
  • To determine if GM-Mφ adopt M2 characteristics after encountering apoptotic neutrophils.

Main Methods:

  • GM-Mφ were preincubated with apoptotic neutrophils (resulting in GM-MφNeu).
  • Phenotypic analysis included CD206 and FasL expression.
  • Functional assays assessed T-cell proliferation and cytokine secretion (27-plex analysis).
  • Prostaglandin E2 (PGE2) synthesis was measured, and its inhibition using indomethacin was tested.

Main Results:

  • GM-MφNeu exhibited increased CD206 and FasL expression, indicative of M2 features.
  • GM-MφNeu showed a reduced capacity to stimulate allogeneic T-cell proliferation.
  • A significant down-regulation of 24 cytokines, including IL-10, was observed in GM-MφNeu.
  • Apoptotic neutrophils enhanced PGE2 synthesis by GM-Mφ.
  • Blocking PGE2 production restored the allostimulatory activity of GM-MφNeu.

Conclusions:

  • GM-Mφ acquire M2 cell features upon exposure to apoptotic cells.
  • GM-MφNeu resemble deactivated (M2c) macrophages due to global cytokine suppression.
  • The inhibition of allogeneic T-cell proliferation by GM-MφNeu is primarily mediated by enhanced PGE2 synthesis, not IL-10.
Keywords:
Allostimulatory activityApoptotic neutrophilsCytokinesMacrophage polarizationPGE2

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