IL‐13 over‐expression in skin is not confined to IgE‐mediated skin inflammation
IL‐13 is produced by T cells and, like IL‐4, it can induce the production of IgE and IgG4. In order to investigate if IL‐13 is a specific marker for atopic dermatitis (AD), IL‐13 gene expression was analysed in chronic lichenified lesions and non‐lesional skin of patients with AD, in involved and non‐involved skin of patients with psoriasis, in positive tuberculin reactions in non‐atopics, and in the skin of healthy control subjects. Patients with AD (n = 9) showed sensitization to common air‐borne allergens (positive Phadiatop) and had total serum IgE values in the range from 10 to 4800 kU/l (median 170 kU/l ). Competitive reverse transcription‐polymerase chain reaction (RT‐PCR) was used to assess IL‐13 gene expression in skin biopsy specimens. IL‐13 gene expression was markedly higher in chronic lichenified lesions of patients with AD (P < 0.01), and in the positive tuberculin reactions (P < 0.01; n = 12) than in skin from healthy control subjects (n = 10). However, there was no significant difference in IL‐13 gene expression in the skin of patients with psoriasis (n = 10) and that of healthy control subjects. The dermal cell infiltrates were larger and the relative amount of CD3+ and CD4+ cells in these infiltrates was higher in the skin of subjects with a positive tuberculin reaction than in lichenified AD skin. However, these differences were not reflected in differences in IL‐13 gene expression. Different triggers of IL‐13 gene expression may influence the diverse patterns of inflammation seen in different inflammatory skin disorders.