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Both the inborn and acquired immune system plays an important role in the pathogenicity of atopic dermatitis (AD). The skin lesions are mostly due to the complex interaction of the cytokines, above all the ones secreted by the T helper 2 lymphocytes (Th2). In the acute phase of the disease, the most important cytokines are IL-4, IL-5 and IL-13, and also the subsequent activation of mastocytes and eosinophiles. The next step is the production of antigen-specific antibodies. The Th2 immune response is initiated by IL-1, IL-25, IL-17, IL-33 and by thymic stromal lymphopoietin (TSLP). Th2 cytokines block the expression of differentiation of certain proteins, like locrine, filaggrin, involucrin, and at the same time, they reduce the beta-antimicrobial peptide levels, disturbing the skin barrier in the process. In the chronic phase of the illness, the Th2 cytokines are predominant, with varying levels of T helper 17 cytokines.
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Duca et al. (2021) studied this question.
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