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.
Highlights
Atopic dermatitis (AD) is a chronic, inflammatory skin disease which is characterized by severe itchiness
In addition to the Th2-dependent response, the influence on inflammation in the skin of patients suffering from atopic dermatitis exerts well-known Th2 lymphocytes, Th17 and Th22 lymphocytes releasing, among others, such cytokines as: IL-17, IL-19, and IL-22 [4,5]
The increase in TSLP production in keratinocytes is affected by both physical epidermis and Staphylococcus aureus, which colonizes the skin in 90% of AD patients [26,27,28,29,30]
Summary
Atopic dermatitis (AD) is a chronic, inflammatory skin disease which is characterized by severe itchiness. Special attention has been paid to immunological factors of Atopic dermatitis (AD) pathogenesis, in addition to epidermal barrier defects. They include numerous disorders of Th2 lymphocytes and the cytokines released by them, IL-4, IL-5, IL-13, and lead to elevated production of IgE, increased inflammation in the skin, and aggravate the skin barrier defect in AD [3]. We will take a closer look at new cytokines: IL-17, IL-19, IL-33, and thymic stromal lymphopoietin, whose role in the development of AD and probably other atopic diseases is gaining importance These cytokines give hope in the field of pathogenesis, and the search for potential genetic/molecular/biological markers among them. This work will indicate the potential area of these cytokines in the treatment of AD in the future (Figure 1)
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