Altering the Th1/Th2 balance as a therapeutic strategy in asthmatic diseases.
The identification of distinct T helper (Th)-cell subsets that differ in cytokine production and effector functions not only provides a framework for normal immune responses to infection and injury, but also for many disease processes. Studies in both humans and animals indicate that airway inflammation in allergic asthma is orchestrated by CD4+ Th2-cells that secrete the cytokines IL-4, IL-5 and IL-13. Many studies also suggest that IFN gamma, secreted by Th1-cells, suppresses the development and effector functions of Th2-cells. Cross-regulation of Th1/Th2 responses has been demonstrated in many experimental systems including models of allergic inflammation/asthma. A challenging concept that has evolved as a result is the use of therapeutic modalities that will modulate the Th1/Th2 balance in asthma without deleterious side effects. In the clinical trial arena, the unmet challenging goal remains to convert the concept of Th1/Th2 balance modulation, without deleterious side effects, into clinical practice for the management of asthmatic disease.
Ray
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Department of Internal Medicine, Yale University School of Medicine, 333 Cedar Street, 105 LCI, New Haven, CT 06520-8057, USA. Anuradha.Ray@yale.edu
Cohn
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D000818:Animals; D018927:Anti-Asthmatic Agents / Q000494:pharmacology*; D001249:Asthma / Q000188:drug therapy* / Q000235:genetics / Q000503:physiopathology; D002454:Cell Differentiation / Q000187:drug effects; D006801:Humans; D006377:T-Lymphocytes, Helper-Inducer / Q000187:drug effects / Q000502:physiology*
D018927:Anti-Asthmatic Agents