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Related Experiment Videos

Complement regulates inhalation tolerance at the dendritic cell/T cell interface.

Jörg Köhl1, Marsha Wills-Karp

  • 1Division of Molecular Immunology, Cincinnati Children's Hospital Medical Center and University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA. ioerg.koehl@chmcc.org

Molecular Immunology
|August 8, 2006
PubMed
Summary

Complement C5a receptor signaling is crucial for maintaining inhalation tolerance in the lungs. Its absence during allergen exposure paradoxically enhances allergic asthma by impairing regulatory T cell function.

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Area of Science:

  • Immunology
  • Allergy Research
  • Pulmonary Medicine

Background:

  • Inhalation tolerance to aeroallergens is normally maintained by pulmonary dendritic cells (DCs) and regulatory T cells (Tregs).
  • Asthma involves a breakdown of this tolerance, leading to Th2-biased airway inflammation.
  • The role of innate immune mediators, like complement, in allergic asthma is under investigation.

Purpose of the Study:

  • To investigate the role of the complement C5a receptor (C5aR) in allergic sensitization and asthma development.
  • To elucidate the mechanisms by which C5aR signaling influences pulmonary immune cells.

Main Methods:

  • Utilized mouse models of experimental allergic asthma.
  • Examined the effects of ablating C5aR signaling on allergen exposure.

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  • Assessed the function of pulmonary dendritic cells and regulatory T cells.

    • Main Results:

    • Ablation of C5aR signaling during initial allergen exposure enhanced Th2 sensitization.
    • C5aR signaling directly impacts pulmonary DC subsets involved in adaptive immunity.
    • C5aR signaling influences Treg-mediated suppression of DC activation and Th2 inflammation.

    Conclusions:

    • Constitutive C5a generation and C5aR signaling in airway DCs are essential for maintaining inhalation tolerance.
    • C5aR signaling controls tolerance both directly and indirectly via Treg sensitization.
    • Dysregulation of C5aR signaling may contribute to the breakdown of tolerance in allergic asthma.