Similar T helper Th2-like cytokine mRNA expression in vernal keratoconjunctivitis regardless of atopic constitution
Article first published online: 23 APR 2002
Volume 57, Issue 5, pages 436–441, May 2002
How to Cite
Montan, P. G., Scheynius, A. and Van Der Ploeg, I. (2002), Similar T helper Th2-like cytokine mRNA expression in vernal keratoconjunctivitis regardless of atopic constitution. Allergy, 57: 436–441. doi: 10.1034/j.1398-9995.2002.13375.x
- Issue published online: 23 APR 2002
- Article first published online: 23 APR 2002
- Accepted for publication 2 November 2001
- gene expression;
Background: Many patients with vernal keratoconjunctivitis (VKC), a severe chronic allergic eye disease in children, exhibit IgE-sensitization, but about 40% of cases lack this immunologic trait. As a disease factor in VKC, IgE is thus not fully understood. The aim of this study was to investigate whether there are any differences in the conjunctival cytokine messenger (m)RNA pattern related to IgE-sensitization in children suffering from VKC.
Methods: Tissue samples were obtained from 16 symptomatic VKC subjects with sub-tarsal disease and six control subjects. Expression of mRNA for interleukin (IL)-4, IL-5, IL-13, and interferon (IFN)-γ was investigated with a semiquantitative reverse-transcriptase polymerase chain reaction (RT-PCR) technique. The presence of T cells, IgE+ cells, mast cells, and eosinophils was analyzed with immunohistochemical methods. Allergen-specific IgE antibodies were assessed in serum and with skin prick testing.
Results: Ten out of the 16 VKC subjects showed evidence of IgE-sensitization. No differences were detected for any tissue variable between VKC subjects with and without IgE-sensitization. Statistically significant increases over controls were found for both VKC groups with regard to all cell markers.
Conclusions: The amount of messenger RNA encoding cytokines and inflammatory cell markers in VKC did not correlate with IgE-sensitization. Tissue changes in all patient samples were characterized by a prevalence of T cells, eosinophils, mast cells and cell-bound IgE molecules. However, the role of cell-bound IgE molecules in VKC patients lacking IgE-sensitization remains to be determined.