Correlation of house dust mite-specific lymphocyte proliferation with IL-5 production, eosinophilia, and the severity of symptoms in infants with atopic dermatitis

J Allergy Clin Immunol. 1998 Jan;101(1 Pt 1):84-9. doi: 10.1016/S0091-6749(98)70197-6.

Abstract

Because house dust mite (HDM)-specific IgE antibody (IgE-RAST) is usually not detectable in infants with atopic dermatitis (AD), HDM has not been regarded as the cause of infantile AD. The level of HDM-specific lymphocyte proliferation (expressed as stimulation index measured by flow cytometry [SIF]), however, was found to be markedly elevated in AD infants. This suggests that the sensitization of T cells to HDM extract occurs even in infancy. Moreover, the level of HDM-SIF is correlated closely with the severity of infantile AD, suggesting that HDM is a major cause of this disease not only in adults and children but also in infants. Although the level of HDM-SIF did not correlate with the level of HDM-specific IgE-RAST in infants with AD, it did intimately correlate with the absolute number of peripheral blood eosinophils. Because T lymphocytes are known to secrete some cytokines, such as IL-5, that enhance the proliferation of eosinophils, we measured the IL-5 production by peripheral blood mononuclear cells in infants with AD on stimulation with HDM extract. The amount of IL-5 production is significantly higher in infants with AD, as well as in children with AD, than that found in nonatopic control subjects. Moreover, the level of IL-5 production is correlated closely with the level of HDM-SIF in infants with AD. Taken together, these results suggest that HDMs play an important role in the development of infantile AD by inducing IL-5 production from HDM-specific T lymphocytes.

MeSH terms

  • Adolescent
  • Adult
  • Age Factors
  • Allergens / adverse effects
  • Animals
  • Candida albicans / immunology
  • Child
  • Child, Preschool
  • Dermatitis, Atopic / etiology*
  • Dermatitis, Atopic / immunology
  • Dust / adverse effects*
  • Eosinophilia / etiology*
  • Eosinophilia / immunology
  • Humans
  • Immunoglobulin E / blood
  • In Vitro Techniques
  • Infant
  • Interleukin-5 / biosynthesis*
  • Lymphocyte Activation*
  • Mites / immunology*

Substances

  • Allergens
  • Dust
  • Interleukin-5
  • Immunoglobulin E