Polyclonal and allergen-induced cytokine responses in children with elevated immunoglobulin E but no atopic disease
Article first published online: 6 NOV 2002
Clinical & Experimental Allergy
Volume 32, Issue 11, pages 1552–1557, November 2002
How to Cite
Smart, J. M., Tang, M. L. K. and Kemp, A. S. (2002), Polyclonal and allergen-induced cytokine responses in children with elevated immunoglobulin E but no atopic disease. Clinical & Experimental Allergy, 32: 1552–1557. doi: 10.1046/j.1365-2222.2002.01532.x
- Issue published online: 6 NOV 2002
- Article first published online: 6 NOV 2002
- Submitted 23 October 2001; revised 14 May 2002; accepted 24 June 2002
- house dust mite;
- rye grass pollen;
Background Reduced Th1 and elevated Th2 cytokine responses are considered to be a principal mechanism in the generation of the inflammation leading to the manifestations of atopic disease in the skin of atopic dermatitis and in the airways of asthma. If reduced Th1 and elevated Th2 responses are principal determinants of the manifestation of atopic disease it might be expected that subjects with established disease would exhibit differences in their cytokine profiles as compared with atopic patients without clinical disease.
Objective To determine whether asymptomatic atopic children exhibit a cytokine imbalance similar to that seen in patients with established atopic disease or if they behave like non-atopic controls. Cytokine responses in a group of children with elevated IgE but no clinical manifestations of disease, atopic children with established disease and non-atopic controls were compared.
Methods We examined allergen-induced (house dust mite, HDM, rye grass pollen and RYE) cytokine responses in parallel with polyclonal (staphylococcal enterotoxin B, SEB) cytokine responses in a group of children with elevated serum IgE levels without current or past evidence of atopic disease (median age 6.6 years) and compared these with a non-atopic control group (median age 6.5 years) and a group of children with atopic disease (median age 6.7 years).
Results Symptomatic atopic children had reduced SEB-induced IFN-γ and increased SEB-induced IL-4 and IL-5 as compared with non-atopic controls. In contrast, SEB-induced IFN-γ, IL-4 and IL-5 production in asymptomatic atopics was not significantly different from the non-atopic control subjects. Allergen-induced Th1 (IFN-γ) and Th2 (IL-5 and IL-13) cytokine production was increased in both symptomatic atopics and asymptomatic atopics when compared with non-atopic controls.
Conclusion The defect in polyclonally induced IFN-γ production was associated with the clinical manifestation of atopic disease but not the atopic state per se. This suggests that the global reduction in IFN-γ is the key determinant of the development of overt atopic disease. In contrast, elevated allergen-induced Th2 cytokine responses in children related to the atopic state per se irrespective of the presence of clinical atopic disease.