Interaction of human peripheral blood monocytes with apoptotic polymorphonuclear cells
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Updated: Jun 20, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
Published on: December 27, 2016
Tomasz P Mikołajczyk1, Joanna E Skrzeczyńska-Moncznik, Mirosław A Zarebski
1Department of Immunology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Gronostajowa, Cracow, Poland. to.mik@interia.pl
Abstract:
Macrophages have the potential to recognize apoptotic neutrophils and phagocytose them while the same function for monocytes is uncertain. In fact, early findings indicated that monocytes started to phagocytose neutrophils on the third day of differentiation to macrophages. Here we show, using flow cytometry and confocal microscopy, that peripheral blood monocytes phagocytose apoptotic but not freshly isolated granulocytes. Recognition of apoptotic cells is predominantly connected with CD16(+) monocytes (CD14(high) CD16(+) and CD14(dim) CD16(+)) and requires CD36. Clearance of apoptotic polymorphonuclear leucocytes appears to be independent of the CD14 mechanism. Uptake of apoptotic Jurkat T cells by monocytes is CD14 and CD36 dependent. Liposomes containing phosphatidyl-l-serine reduce binding of apoptotic polymorphonuclear leucocytes. Lipopolysaccharide-activated subpopulations of monocytes while in contact with apoptotic cells produce more anti-inflammatory cytokine interleukin-10 whereas the production of pro-inflammatory cytokines, tumour necrosis factor-alpha and interleukin-1beta is reduced.
Insights
Peripheral blood monocytes phagocytose apoptotic neutrophils, a process mediated by CD36. This phagocytosis involves specific monocyte subsets and results in reduced pro-inflammatory cytokine production.
Area of Science:
- Immunology
- Cell Biology
Background:
- Macrophages phagocytose apoptotic neutrophils, but monocyte function is less understood.
- Previous studies suggested monocytes require differentiation into macrophages to phagocytose neutrophils.
Purpose of the Study:
- To investigate the phagocytic capacity of peripheral blood monocytes for apoptotic neutrophils.
- To identify the specific monocyte subsets and molecular mechanisms involved in phagocytosis.
Main Methods:
- Flow cytometry and confocal microscopy were employed.
- Analysis focused on CD14 and CD16 monocyte subsets.
- Investigated the role of CD36 and phosphatidyl-L-serine.
Main Results:
- Peripheral blood monocytes phagocytose apoptotic, but not live, granulocytes.
- CD16(+) monocyte subsets (CD14(high)CD16(+) and CD14(dim)CD16(+)) are primarily involved.
- Phagocytosis requires CD36 and is independent of the CD14 mechanism for neutrophils.
- Uptake of apoptotic Jurkat T cells is CD14 and CD36 dependent.
- Phosphatidyl-L-serine liposomes reduced binding of apoptotic neutrophils.
- Lipopolysaccharide-activated monocytes produced more IL-10 and less TNF-α and IL-1β upon contact with apoptotic cells.
Conclusions:
- Monocytes directly phagocytose apoptotic neutrophils via CD36-dependent pathways.
- Specific CD16(+) monocyte subsets mediate this clearance.
- Monocyte interaction with apoptotic cells modulates cytokine production, favoring an anti-inflammatory response.
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