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IL-3 up-regulates and activates human eosinophil CD32 and αMβ2 integrin causing degranulation.

S Esnault1, M W Johansson2, E A Kelly1

  • 1Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI, USA.

Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology
|December 22, 2016
PubMed
Summary

Interleukin-3 (IL-3) significantly enhances eosinophil degranulation by upregulating CD32B/C receptors and αMß2 integrin, impacting inflammatory diseases like asthma. This finding reveals IL-3 as a key mediator in eosinophil activation.

Keywords:
CD32IL-3allergen challengedegranulationeosinophils

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Medicine

Background:

  • Eosinophils play a crucial role in diseases such as asthma.
  • Targeting IL-5 or its receptor reduces asthma exacerbations.
  • IL-3, IL-5, and GM-CSF share a common beta-chain for eosinophil receptors; IL-3 is more potent in promoting protein translation via ERK/p90S6K/RPS6 signaling.

Purpose of the Study:

  • To investigate the disease-relevant effects of prolonged eosinophil stimulation with IL-3.

Main Methods:

  • Human blood eosinophils were utilized to assess IL-3's impact on IgG-driven degranulation.
  • Comparison of IL-3's effects against IL-5 and GM-CSF on eosinophil activation markers (CD32, αMß2 integrin, CD32B/C, CD32A).
  • In vitro findings were validated in vivo on airway eosinophils.

Main Results:

  • IL-3 exposure, compared to IL-5, further induced eosinophil degranulation on aggregated IgG.
  • IL-3 increased the production and activation of CD32 (low-affinity IgG receptor) and αMß2 integrin.
  • IL-3 uniquely induced CD32B/C protein expression without altering CD32A protein or CD32B/C mRNA levels.
  • In vitro observed changes were recapitulated in vivo on airway eosinophils.

Conclusions:

  • This study demonstrates, for the first time, the upregulation of CD32B/C on eosinophils.
  • IL-3 is identified as a potent inducer of eosinophil degranulation mediated by CD32 and αMß2 integrin.
  • These findings highlight IL-3's significant role in eosinophil activation and potential implications for inflammatory diseases.