Novel fundamental approaches to intervening in IgE-mediated allergic diseases

J Invest Dermatol. 1994 Feb;102(2):141-4. doi: 10.1111/1523-1747.ep12371750.


Recent progress in our understanding of the immunologic basis of allergic diseases has suggested that enhanced production of the cytokines IL-4 and IL-13 by allergen-specific T cells is responsible for increased IgE synthesis and the development of allergic disease in certain individuals. Based on these observations, it is clear that approaches to inhibition of allergen-specific IgE synthesis should be aimed at blocking the activation or preventing the synthesis of IL-4 and IL-13. In the present review, two approaches toward this goal are discussed. First, an IL-4 mutant protein is described that acts as a powerful antagonist of both IL-4 and IL-13 activity, including induction of IgE synthesis by these cytokines in vitro. Second, it is demonstrated that T-cell clones can be rendered non-responsive following incubation with allergen-derived peptides representing minimal T-cell activation-inducing epitopes. These non-responsive T cells fail to produce IL-4 and IL-13 and to proliferate following subsequent activation with the relevant allergen and antigen-presenting cells. In addition, these non-responsive T cells fail to provide B-cell help for IgE synthesis. It is tempting to speculate that induction of non-responsiveness in allergen-specific T-cell clones by allergen-derived immunogenic peptides may provide the basis for successful desensitization of allergic patients.

Publication types

  • Review

MeSH terms

  • Desensitization, Immunologic
  • Humans
  • Hypersensitivity / etiology*
  • Hypersensitivity / metabolism
  • Hypersensitivity / physiopathology*
  • Immunoglobulin E / metabolism
  • Immunoglobulin E / physiology*
  • Interleukin-3 / metabolism
  • Interleukin-3 / physiology
  • Interleukin-4 / metabolism
  • Interleukin-4 / physiology
  • T-Lymphocytes / immunology
  • T-Lymphocytes / metabolism
  • T-Lymphocytes / physiology


  • Interleukin-3
  • Interleukin-4
  • Immunoglobulin E