Source: Allergy  |  Posted 9 years ago

Interleukin-13 (IL-13) may be a key cytokine in the pathogenesis of both IgE-associated and non-IgE-associated forms of allergic atopic eczema/dermatitis syndrome (AEDS).

Swiss researchers say the underlying mechanism leading to increased differentiation of T helper 2 cells may involve a deficit capacity to produce interferon-gamma (IFN-gamma) in IgE-associated AEDS patients. But, they did not find this deficit capacity in non-IgE-associated AEDS patients.

Non-IgE-associated AEDS patients have normal total and specific IgE levels and negative skin-prick tests toward common environmental allergens.

Investigators from the University of Bern and the Clinic for Dermatology and Allergy in Davos compared cytokine production patterns of peripheral blood mononuclear cells (PBMCs) in patients with both types of AEDS and in healthy controls.

Stimulated PBMCs from IgE-associated patients produced less IFN-gamma when compared with stimulated PBMCs from non-IgE-associated AEDS patients and controls. "However, stimulated PBMCs from both IgE-associated AEDS and non-IgE-associated AEDS patients produced more IL-13 than PBMCs from control individuals," the researchers explain.

They note that IL-5 production was significantly increased in non-IgE-associated AEDS patients but not in IgE-associated patients.