Impact of interleukin-17 on macrophage phagocytosis of apoptotic neutrophils and particles

Inflammation. 2011 Feb;34(1):1-9. doi: 10.1007/s10753-010-9201-8.


There is now substantial evidence that the cytokine interleukin-17 orchestrates the accumulation of neutrophils in mammals and thereby contributes to host defense. However, the role of IL-17 in controlling neutrophil turnover is not fully understood. Here, we demonstrate that IL-17 stimulates the apoptosis of mouse neutrophils and, simultaneously, the release of the microbicidal compound, myeloperoxidase. IL-17 also stimulates mouse macrophages to phagocytose aged neutrophils and latex beads, and it induces an increase in a soluble form of the phagocytic receptor, lectin-like oxidized low-density lipoprotein receptor-1 as well. In contrast, IL-17 does not markedly increase the release of the archetype neutrophil-recruiting cytokine, macrophage inflammatory protein-2 in mouse macrophages. Importantly, IL-17 also stimulates the phagocytosis of latex beads in human monocyte-derived macrophages. Thus, IL-17 bears the potential to control both phagocytosis and neutrophil turnover during activation of host defense.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / immunology*
  • Apoptosis / physiology
  • Cells, Cultured
  • Enzyme-Linked Immunosorbent Assay
  • Fluorescent Antibody Technique
  • Humans
  • Interleukin-17 / immunology*
  • Macrophage Inflammatory Proteins / biosynthesis
  • Macrophages / immunology*
  • Macrophages / metabolism
  • Mice
  • Mice, Inbred BALB C
  • Microspheres
  • Neutrophils / immunology*
  • Neutrophils / metabolism
  • Peroxidase / metabolism
  • Phagocytosis / immunology*
  • Phagocytosis / physiology
  • Scavenger Receptors, Class E / biosynthesis


  • Interleukin-17
  • Macrophage Inflammatory Proteins
  • Scavenger Receptors, Class E
  • Peroxidase