Early pediatric atopic dermatitis shows only a cutaneous lymphocyte antigen (CLA) 1 TH2/TH1 cell imbalance, whereas adults acquire CLA1+ TH22/TC22 cell subsets

Background: Identifying differences and similarities between cutaneous lymphocyte antigen (CLA)(+) polarized T-cell subsets in children versus adults with atopic dermatitis (AD) is critical for directing new treatments toward children. Objective: We sought to compare activation markers and frequencies of skin-homing (CLA(+)) versus systemic (CLA(-)) "polar'' CD4 and CD8 T-cell subsets in patients with early pediatric AD, adults with AD, and control subjects. Methods: Flow cytometry was used to measure CD69/inducible costimulator/HLA-DR frequency in memory cell subsets, as well as IFN-gamma, IL-13, IL-9, IL-17, and IL-22 cytokines, defining T(H)1/cytotoxic T(T-C) 1, T(H)2/T(C)2, TH9/T(C)9, T(H)17/T(C)17, and T(H)22/T(C)22 populations in CD4 and CD8 cells, respectively. We compared peripheral blood from 19 children less than 5 years old and 42 adults with well-characterized moderate-to-severe AD, as well as age-matched control subjects (17 children and 25 adults). Results: Selective inducible costimulator activation (P <. 001) was seen in children. CLA(+)T(H)2 T cells were markedly expanded in both children and adults with AD compared with those in control subjects, but decreases in CLA(+)T(H)1 T-cell numbers were greater in children with AD (17% vs 7.4%, P = .007). Unlike in adults, no imbalances were detected in CLA(-) T cells from pediatric patients with AD nor were there altered frequencies of T(H)22 T cells within the CLA(+) or CLA(-) compartments. adults with AD hAD increased frequencies of IL-22-producing CD4 and CD8 T cells within the skin-homing population, compared with controls (9.5% vs 4.5% and 8.6% vs 2.4%, respectively; P <. 001), as well as increased HLA-DR activation (P < .01). Conclusions: These data suggest that T(H)2 activation within skin-homing T cells might drive AD in children and that reduced counterregulation by T(H)1 T cells might contribute to excess T(H)2 activation. T(H)22 "spreading'' of AD is not seen in young children and might be influenced by immune development, disease chronicity, or recurrent skin infections.