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Apoptotic neutrophils and T cells sequester chemokines during immune response resolution through modulation of CCR5

Amiram Ariel1, Gabrielle Fredman, Yee-Ping Sun

  • 1Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.

Nature Immunology
|October 3, 2006
PubMed

Insights

During inflammation resolution, apoptotic leukocytes expressing CCR5 clear chemokine signals. This study reveals CCR5+ apoptotic cells terminate chemokine signaling, aiding inflammation resolution.

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Inflammation resolution involves clearing apoptotic cells by macrophages.
  • Chemokine signaling plays a role in inflammatory processes.

Purpose of the Study:

  • To investigate the role of the CCR5 chemokine receptor in the resolution of inflammation.
  • To identify the function of CCR5 expression on apoptotic leukocytes during inflammation resolution.

Main Methods:

  • Utilized CCR5-deficient mice to study peritonitis resolution.
  • Analyzed the expression of CCR5 on apoptotic neutrophils and T cells.
  • Investigated the regulation of CCR5 expression by inflammatory and proresolution mediators in human polymorphonuclear cells.

Main Results:

  • CCL3 and CCL5 chemokines persisted in CCR5-deficient mice during inflammation resolution.
  • CCR5 expression on apoptotic leukocytes sequestered and cleared CCL3 and CCL5.
  • Proinflammatory stimuli downregulated CCR5 on apoptotic cells, while proresolution mediators upregulated it.

Conclusions:

  • CCR5+ apoptotic leukocytes act as 'terminators' of chemokine signaling.
  • CCR5-mediated clearance of chemokines contributes to the resolution of inflammation.
  • Regulation of CCR5 on apoptotic cells by inflammatory and proresolution mediators is crucial.

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