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CCL5 Promotes Resolution-Phase Macrophage Reprogramming in Concert with the Atypical Chemokine Receptor D6 and

Miran Aswad1,2, Simaan Assi1,2, Sagie Schif-Zuck1,2

  • 1Department of Biology, Faculty of Natural Sciences, University of Haifa, Haifa 3498838, Israel; and.

Journal of Immunology (Baltimore, Md. : 1950)
|July 5, 2017
PubMed

Insights

The chemokine CCL5, when bound to apoptotic neutrophils expressing D6, reprogrammes macrophages to reduce inflammation. This D6-dependent interaction is crucial for resolving inflammation.

Area of Science:

  • Immunology
  • Inflammation Resolution

Background:

  • Apoptotic polymorphonuclear cell (PMN) engulfment reprograms macrophages to reduce inflammation.
  • The atypical chemokine receptor D6/ACKR2 on apoptotic PMN regulates macrophage reprogramming.

Purpose of the Study:

  • To investigate the role of chemokine CCL5 in macrophage reprogramming during inflammation resolution.
  • To determine the involvement of D6 receptor in CCL5-mediated macrophage reprogramming.

Main Methods:

  • Investigated CCL5 retention during zymosan A peritonitis resolution in mice.
  • Assessed CCL5 secretion by resolution-phase macrophages.
  • Evaluated CCL5's effect on macrophage reprogramming in vivo (D6+/+ and D6-/- mice) and ex vivo with apoptotic PMN.

Main Results:

  • CCL5 was largely retained (75%) during inflammation resolution.
  • CCL5 promoted macrophage reprogramming in D6+/+ mice but not D6-/- mice.
  • CCL5 enhanced macrophage reprogramming ex vivo only when bound to D6+/+ apoptotic PMN, activating p38MAPK and JNK signaling.

Conclusions:

  • CCL5 plays a novel pro-resolving role on macrophages.
  • This function of CCL5 is dependent on its interaction with D6 expressed on apoptotic PMN.

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