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Related Experiment Video

Updated: Jul 17, 2026

A Reversible, Non-invasive Method for Airway Resistance Measurements and Bronchoalveolar Lavage Fluid Sampling in Mice
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Prolonged inhaled allergen exposure can induce persistent tolerance.

Chris L Van Hove1, Tania Maes, Guy F Joos

  • 1Department of Respiratory Diseases, Faculty of Medicine, Ghent University and Ghent University Hospital 7K12 I.E., De Pintelaan 185, 9000 Ghent, Belgium.

American Journal of Respiratory Cell and Molecular Biology
|January 16, 2007
PubMed
Summary

Persistent allergen exposure induces immune tolerance in murine asthma models, resolving airway inflammation. This tolerance involves altered dendritic cell-T cell interactions and offers long-lasting protection against allergic responses.

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Area of Science:

  • Immunology
  • Allergy and Asthma Research
  • Immune Tolerance Mechanisms

Background:

  • Allergic airway disease is often linked to Th2 immunity, but tolerance failure may be key.
  • Prolonged allergen exposure can paradoxically resolve inflammation, a mechanism yet to be elucidated.
  • Altered dendritic cell-T cell interactions are hypothesized to drive this resolution.

Purpose of the Study:

  • Investigate the mechanisms behind the waning of Th2-driven airway inflammation upon prolonged antigen exposure.
  • Determine if this resolution is associated with immune tolerance induction.
  • Characterize the cellular and molecular changes involved in the inhibition of allergic airway disease.

Main Methods:

  • Established a murine model of Th2-driven airway disease.
  • Administered prolonged ovalbumin (OVA) exposure (8 weeks) to induce tolerance.
  • Assessed immune responses, including cellular infiltration, antibody levels, cytokine production, and regulatory cell populations.
  • Analyzed dendritic cell (DC) maturation and T cell co-stimulatory molecule expression.

Main Results:

  • Prolonged OVA exposure completely resolved airway inflammation.
  • Re-challenge failed to elicit Th2-skewed responses, indicating specific immune tolerance.
  • Bystander protection against unrelated antigens was observed.
  • Decreased regulatory T cells (CD4+CD25+Foxp3+), PD-1, IL-10, ICOS, and CD28 expression were noted.
  • Inhibited DC maturation was observed, distinct from TLR-4 signaling.

Conclusions:

  • Persistent antigen exposure induces antigen-specific, long-lasting immune tolerance in Th2-driven airway disease.
  • This tolerance is characterized by altered DC-T cell communication.
  • The observed disease inhibition mechanism differs from acute anti-inflammatory responses.