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Review
. 2018 Oct 9;19(10):3086.
doi: 10.3390/ijms19103086.

New Cytokines in the Pathogenesis of Atopic Dermatitis-New Therapeutic Targets

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Review

New Cytokines in the Pathogenesis of Atopic Dermatitis-New Therapeutic Targets

Jolanta Klonowska et al. Int J Mol Sci. .

Abstract

Atopic dermatitis (AD) is a recurrent, chronic, and inflammatory skin disease, which processes with severe itchiness. It often coexists with different atopic diseases. The number of people suffering from AD is relatively high. Epidemiological research demonstrates that 15⁻30% of children and 2⁻10% adults suffer from AD. The disease has significant negative social and economic impacts, substantially decreasing the quality of life of the patients and their families. Thanks to enormous progress in science and technology, it becomes possible to recognise complex genetic, immunological, and environmental factors and epidermal barrier defects that play a role in the pathogenesis of AD. We hope that the new insight on cytokines in AD will lead to new, individualised therapy and will open different therapeutic possibilities. In this article, we will focus on the cytokines, interleukin (IL)-17, IL-19, IL-33, and TSLP (thymic stromal lymphopoietin), which play a significant role in AD pathogenesis and may become the targets for future biologic therapies in AD. It is believed that the new era of biological drugs in AD will give a chance for patients to receive more successful treatment.

Keywords: IL-17; IL-19; IL-33; TSLP; atopic dermatitis; biological agents; cytokines.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Schematic summary of immunological disorders in Atopic dermatitis (AD) pathogenesis coexisting with skin barrier defect. The diagram shows inflammatory cells, Th2, Th17, and Th22-dependent inflammation in AD with cytokines, which diminish the epidermal barrier. The impact of infections, allergens, stress, and itchiness, leading to the activation of inflammatory pathways. The figure depicts the possible targets of biological agents in AD treatment. DC (dendritic cells), EOS (eosinophil), FLG (filaggrin), IL (interleukin), IFN-α (interferon-alfa), IFN-γ (interferon gamma), ILC (lymphoid cells), MC (mast cells), TGF-β (transforming growth factor beta), TSLP (thymic stromal lymphopoietin). X—indicates potential areas of new biological drugs action.

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