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The Atypical Chemokine Receptor Ackr2 Constrains NK Cell Migratory Activity and Promotes Metastasis

Christopher A H Hansell1, Alasdair R Fraser1, Alan J Hayes1

  • 1Chemokine Research Group, Institute of Infection, Immunity, and Inflammation, University of Glasgow, Glasgow G12 8TA, United Kingdom.

Journal of Immunology (Baltimore, Md. : 1950)
|August 31, 2018
PubMed

Insights

Mice lacking atypical chemokine receptor Ackr2 showed reduced metastasis. This was due to enhanced natural killer (NK) cell activity against tumors, mediated by increased chemokine receptor CCR2 expression on NK cells.

Area of Science:

  • Immunology
  • Cancer Biology
  • Molecular Biology

Background:

  • Chemokines play crucial roles in cancer progression and metastasis.
  • Atypical chemokine receptors (ACKRs) modulate chemokine signals, influencing immune responses.
  • The specific role of ACKR2 in cancer metastasis is not fully understood.

Purpose of the Study:

  • To investigate the role of atypical chemokine receptor Ackr2 in cancer metastasis.
  • To elucidate the mechanisms by which Ackr2 influences anti-tumor immunity.

Main Methods:

  • Utilized knockout mouse models deficient in Ackr2 (Ackr2-/-).
  • Assessed metastasis development in cell line and spontaneous cancer models.
  • Analyzed chemokine receptor expression (CCR2) on natural killer (NK) cells.
  • Quantified NK cell recruitment to tumors and evaluated tumoricidal activity.

Main Results:

  • Ackr2 deficiency led to impaired metastasis in vivo.
  • Ackr2-/- mice exhibited increased expression of chemokine receptor CCR2 on KLRG1+ NK cells.
  • Enhanced recruitment of KLRG1+ NK cells to CCL2-expressing tumors was observed.
  • Increased NK cell activity resulted in enhanced tumor killing.

Conclusions:

  • Ackr2 negatively regulates CCR2 expression on NK cells, thereby limiting their anti-tumor activity.
  • Targeting Ackr2 and CCR2 may represent a novel therapeutic strategy for combating cancer metastasis.

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