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Immune complex-induced haptokinesis in human non-classical monocytes.

Sophie L Preuß1, Stephanie Oehrl1, Hao Zhang1

  • 1Department of Dermatology, University Hospital Heidelberg, Heidelberg, Germany.

Frontiers in Immunology
|March 20, 2023
PubMed
Summary

Immune complexes (ICs) trigger a unique haptokinesis migratory response in specific monocyte subsets, particularly non-classical monocytes (ncMo), offering new insights into autoimmune diseases.

Keywords:
6-sulfo LacNAc+ monocytesADAM17CD16Fc gamma receptorcell migrationhaptokinesisimmune complexesnon-classical monocytes

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Area of Science:

  • Immunology
  • Cell Biology
  • Autoimmune Diseases

Background:

  • Immune complexes (ICs) are implicated in autoimmune diseases, but their precise role in leukocyte migration is often unclear.
  • Leukocyte detection of ICs via IC receptors initiates signaling pathways that influence local immune responses.
  • Understanding IC-mediated cellular behavior is crucial for elucidating autoimmune pathogenesis.

Purpose of the Study:

  • To investigate the specific migratory response of different monocyte subsets to immune complexes (ICs).
  • To elucidate the signaling pathways and molecular mechanisms underlying IC-induced monocyte migration.
  • To explore the potential role of IC-induced haptokinesis in autoimmune disease pathomechanisms.

Main Methods:

  • Live imaging and automated cell tracking to analyze monocyte migration dynamics.
  • Functional assays involving blocking antibodies against CD16 and SYK signaling pathways.
  • Investigation of the role of ADAM17 metalloproteinase activity.
  • Utilizing matrices with defined ligand spacing to assess ligand density effects.

Main Results:

  • ICs induce a distinct haptokinesis migratory response specifically in 6-sulfo LacNAc+ monocytes (slanMo) and non-classical monocytes (ncMo), but not in intermediate (imMo) or classical monocytes (cMo).
  • IC-dependent haptokinesis is characterized by cell elongation, actin polarization, and directional migration, mediated by CD16 and SYK signaling.
  • ADAM17 activity influences IC-dependent haptokinesis, potentially through CD16 cleavage, and ligand density affects the migratory response magnitude.

Conclusions:

  • Immune complexes induce a specific migratory behavior, haptokinesis, in non-classical monocytes.
  • CD16-dependent signaling and ADAM17 activity are key regulators of this IC-induced monocyte migration.
  • This finding provides a foundation for studying IC-dependent haptokinesis in ncMo as a potential pathomechanism in autoimmune diseases.