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Evaluates IL4 expression in cow milk allergy patients, suggesting Th2 dysregulation role.
To examine the potential role of Th1 and Th2 dysregulation in the ethiopathogenesis of cow milk allergy (CMA), here we analysed comparatively IL4 and gamma-interferon (INF γ) expression in peripheral blood mononuclear cells (PBMC) from patients with CMA vs controls. Patients with reaginic CMA (n=5, mean age = 11.6 months), were selected according to the following criteria: clinical symptoms that appeared less than three hours after being fed orally with cow milk challenge and that were curred by a diet free of cow milk elevated serum levels of total IgE and of IgE specific for casein. in vitro induced T cell proliferation in response to the casein antigen PBMC from these patients were in vitro stimulated with the pockweed mitogen (pwd) or the casein antigen (Ag) and cytokine mRNA levels were evaluated by the highly sensitive and semi quantitative RT-PCR cycle method. As controls, PBMC from non allergic patients matched for age (n=3, mean age = 12.6 months) or healthy adults (n = 3) were treated in parallele. Following stimulation with the non specific pwd activator both IL4 and IFN γ mRNAs were induced with similar magnitude in patients and controls. In contrast, following with the casein Ag, a Th2 response, ie an increase of IL4 but not of IFN γ mRNA levels was found in among 5 patients with CMA whereas no cytokins mRNAs were induced in any control individual (0/6). Altogether these results indicate that a Th2 profile of cytokine was selectively induced by the casein Ag in reaginic CMA, therefore suggesting that abnormal Th2 response to cow milk antigen might be responsible for this disease.
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Pélatan et al. (1997) studied this question.
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