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Related Experiment Videos

T cells and chronic asthma.

O M Kon1, A B Kay

  • 1Allergy and Clinical Immunology, National Heart and Lung Institute, Imperial College School of Medicine, London, UK.

International Archives of Allergy and Immunology
|May 4, 1999
PubMed
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Chronic T memory cells drive asthma by releasing cytokines that activate eosinophils, leading to airway damage. Targeting these T cells offers a promising new treatment for asthma.

Area of Science:

  • Immunology
  • Pulmonology
  • Allergy

Background:

  • Asthma pathogenesis involves T memory cells chronically activated by allergens or viruses.
  • These T cells, specifically CD4+ T helper (Th) and CD8+ cytotoxic (Tc) cells, reside in asthmatic airways.
  • A subset of these cells exhibits a type 2 cytokine phenotype (Th-2 and Tc-2).

Purpose of the Study:

  • To investigate the role of chronically activated T memory cells in driving and maintaining the asthma process.
  • To explore the mechanisms by which T cells contribute to airway inflammation and damage in asthma.
  • To identify potential therapeutic targets within T cell pathways for asthma treatment.

Main Methods:

  • Analysis of T cell populations and cytokine expression in asthmatic airways.

Related Experiment Videos

  • Identification of T cell products and mRNA for type 2 cytokines (IL-4, IL-5) in patient biopsies.
  • Assessment of the effects of T cell activation on eosinophil recruitment and activation.
  • Evaluation of the efficacy of immunosuppressive agents (cyclosporin A) and T cell-targeting therapies (anti-CD4) in asthma models or patients.

    • Main Results:

    • Activated T memory cells and their type 2 cytokine products (IL-4, IL-5, GM-CSF) are present in various asthma types (atopic, non-atopic, occupational).
    • These cytokines recruit and activate eosinophils, contributing to airway inflammation, epithelial shedding, mucus hypersecretion, and bronchial muscle contraction.
    • T cells remain activated in corticosteroid-resistant asthma, and disease severity correlates with type 2 cytokines, particularly IL-5.
    • Immunomodulatory therapies targeting T cells show efficacy in chronic, steroid-dependent asthma.

    Conclusions:

    • T cell-mediated immune responses, particularly those involving type 2 cytokines, are central to the pathogenesis of asthma.
    • Eosinophil-mediated mucosal damage in asthma is regulated by T cell activity.
    • Targeting specific T cell molecular pathways represents a promising therapeutic strategy for chronic asthma management.