Clinical and Immunologic Characteristics of Allergen-Specific Immunotherapy in Children with Atopic Dermatitis

Background: The aim was to determine the dynamic of clinical symptoms and saliva concentrations (SC) of IL-4, IL-13, IFNγ in children (Ch) with atopic dermatitis (AD) in the setting of background therapy (BT) and accelerated parenteral allergen-specific immunotherapy (APAI) with house dust mite allergens (HDMA). Methods: The study included a total of 33 Ch with non-acute AD. The mean age at enrollment was 7.2±2.1. The APAI has been provided for 36 months (M) according to accelerated regimen by parenteral introduction of HDMA (2 times/day through 6 h.), along with BT. SC of IL-4, IL-13, IFNγ were measured using ELISA at 1, 3, 6, 12 and 36M after treatment initiation. Results: The efficacy after 12M of APAI was 78.7–84.8% depending on disease severity. The “excellent” result after APAI course was achieved in 21.2% Ch with AD, “good” in 57.6% Ch, “satisfactory” in 9.1% Ch, and there was no therapeutic effect in 12.1% Ch. There was reduction in the number, duration and severity of AD exacerbations observed in 2/3 Ch, which allowed the subsequent reduction of BT. As early as at 6 M there was a 1.5 times decrease of hospitalization number (р<0.05) as compared to the pre-treatment year. After the 1st M of APAI in Ch with AD there was no significant decrease of SC of IL-4, IL-13 and no increase of saliva IFNγ level either (р<0.05). There was no normalization of SC IL-4 and IL-13 during first 6 months in Ch with severe AD as well, though their levels decreased at an average of more than 1.5 times. 12 M of APAI provided duplication of local SC of IFNγ. This saliva IFNγ increase in Ch with AD on the background of APAI was accompanied by decrease of specific IgE against HDMA (r= –0.73). The pre-APAI immune disorder formula was IL-43+IL-132+IFNγ3-IgE3+. After termination of treatment course with HDMA it has changed for IL-42+IL-132+IFNγ1-IgE2+. Conclusions: The results showed that pathogenetic therapy contributes to reduction of SC and inhibits immune inflammation by down regulating  the pro-inflammatory cytokine IL-4 and IL-13 production and activating IFNγ synthesis. Thus the accelerated parenteral APAI is effective in Ch with AD.